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        <title>Frontiers in Physiology | Skeletal Physiology section | New and Recent Articles</title>
        <link>https://www.frontiersin.org/journals/physiology/sections/skeletal-physiology</link>
        <description>RSS Feed for Skeletal Physiology section in the Frontiers in Physiology journal | New and Recent Articles</description>
        <language>en-us</language>
        <generator>Frontiers Feed Generator,version:1</generator>
        <pubDate>2026-05-14T09:55:54.258+00:00</pubDate>
        <ttl>60</ttl>
        <item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1820186</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1820186</link>
        <title><![CDATA[Morphological characteristics of lumbar vertebral bodies and regional distribution patterns of bone mineral density: a CT study]]></title>
        <pubdate>2026-05-14T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Xiaoteng Li</author><author>Fengzi Lv</author><author>Xin Tang</author><author>Peng Jia</author><author>Yang Gao</author>
        <description><![CDATA[ObjectiveTo establish a comprehensive database of the macroscopic morphology and spatial distribution of bone mineral density (BMD) in lumbar vertebral bodies, analyze morphological variation patterns of lumbar structures, and provide reference data for spinal biomechanical modeling and clinical surgery.MethodsA total of 100 healthy volunteers (50 males, 50 females; age range, 20–70 years) who underwent lumbar spine CT evaluation at the Department of Health Examination, Zhengzhou Orthopedic Hospital between September 2023 and September 2025 were retrospectively enrolled in this study. On CT images, seven morphological parameters (anterior, middle, and posterior vertebral body heights; superior and inferior endplate widths; anterior one-third and posterior one-third cortical thickness of the superior endplate) and CT values in 15 different regions (the vertebral body sagittal plane divided into upper, middle, and lower thirds; the horizontal plane divided into anterior, posterior, left, and right quadrants) were measured for each vertebral body from L1 to L5.Results① Morphology: Superior and inferior endplate widths increased progressively from L1 to L5. The relationship between anterior and posterior vertebral body heights showed posterior height > anterior height at L1 and L2, showed no statistically significant difference at L3, and anterior height > posterior height at L4 and L5. The cortical thickness of the anterior one-third of the superior endplate was significantly smaller according to the posterior one-third (P < 0.05). ② CT values: Within vertebral bodies, CT attenuation values showed a gradual increase from the upper one-third to the lower one-third regions. Comparison across segments roughly followed the pattern L1 > L2 > L5 > L3 > L4. Across all segments, the CT value in the anterosuperior region of the vertebral body (anterosuperior region) was the lowest.ConclusionThe morphology of lumbar vertebral bodies demonstrates a consistent morphological trend from L1 to L5 which may be associated with increasing axial loads and contribute to physiological lordosis. There is significant heterogeneity in the distribution of BMD within the vertebral body, with the anterosuperior region identified as a “stress-weak zone, ” highly consistent with the predilection site for clinical compression fractures. The morphological and densitometric database established in this study can provide reference data for spinal surgery planning, implant design, and biomechanical research.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1821673</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1821673</link>
        <title><![CDATA[“Age is associated with Achilles tendon thickness in older adults: an ultrasound case–control study with intra-observer reliability”]]></title>
        <pubdate>2026-05-13T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Jorge Posada-Ordax</author><author>Marta Elena Losa-Iglesias</author><author>Ricardo Becerro de Bengoa-Vallejo</author><author>Eduardo Pérez-Boal</author><author>Bibiana Trevissón-Redondo</author><author>Israel Casado-Hernández</author><author>Antonio Javier Casanova-Malpica</author><author>Eva María Martínez-Jiménez</author><author>Hugo Espigares-Martínez</author><author>Francisco Javier Ruiz-Sánchez</author>
        <description><![CDATA[IntroductionObesity is associated with metabolic, inflammatory, and mechanical alterations that may affect the structure of the Achilles tendon, especially in older adults, who present increased tendon vulnerability due to age-related degenerative changes. To compare the ultrasound thickness of the Achilles tendon between sedentary older adults with obesity and those with normal weight, and to evaluate the intra-observer reliability of ultrasound measurements.MethodsA case–control study was conducted with 120 sedentary older adults (60 obese; 60 normal weight). The thickness of the right Achilles tendon was measured by ultrasound in the longitudinal plane at 4cm from the calcaneal insertion. Each participant was assessed using three consecutive measurements. Groups were compared using the independent samples t-test. Intra-observer reliability was analyzed using ICC (2,1).ResultsThe obese group showed a significantly greater tendon thickness compared with the control group (p = 0.003). However, the obese group was significantly younger than the control group. After adjusting for age in a linear regression model, age was the only significant factor associated with tendon thickness (p = 0.002), whereas obesity lost its significance (p = 0.143). Intra-observer reliability was excellent in both groups (ICC = 0.998 in controls; ICC = 0.986 in obese participants), with low SEM and MDC values.DiscussionUltrasound measurement of Achilles tendon thickness demonstrated excellent intra-observer reliability in sedentary older adults. Although obese participants showed greater tendon thickness in the unadjusted analysis, age was significantly associated with tendon thickness after adjustment, suggesting that aging may play an important role in tendon structural characteristics in this population.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1795836</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1795836</link>
        <title><![CDATA[Effects of chronic sleep deprivation on the bone mineral density, bone microarchitecture and body weight of mice: exploratory study]]></title>
        <pubdate>2026-05-05T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Weiwei Xiang</author><author>Zhen Lv</author><author>Xinwen Min</author><author>Junhao Zhang</author><author>Handong Yang</author><author>Jun Chen</author><author>Jishun Chen</author><author>Dongfeng Li</author><author>Hao Xu</author><author>Chao Luo</author><author>Wenwen Wu</author>
        <description><![CDATA[ObjectiveThis study aimed to investigate the long-term effects of chronic sleep deprivation (CSD) on the bone mineral density (BMD), bone microarchitecture, biomechanical properties and body weight of middle-aged and older male C57BL/6 mice.MethodsTwenty-one 8-month-old mice were randomly assigned to a CSD group (n = 9) or a control group (n = 12). The CSD group was subjected to sleep deprivation using an automated sleep deprivation apparatus for 3 months. Trabecular bone microarchitecture at the distal femur was evaluated by microcomputed tomography. Femoral biomechanical properties were assessed using a three-point bending test, and body weight was monitored weekly throughout the experiment.ResultsThree months of CSD significantly reduced BMD, bone volume (BV) and trabecular thickness (Tb.Th) compared with those of the control group (all P < 0.05). Trabecular separation (Tb.Sp) and bone surface (BS) were also significantly decreased (P < 0.05). No significant differences were observed in trabecular number (Tb.N), bone volume fraction (BV/TV) or other microarchitectural parameters. Three-point bending test showed no statistically significant differences in any biomechanical indices, including maximum load, bending stiffness and elastic modulus (all P > 0.05), between the two groups. Body weight monitoring revealed that the CSD group had significantly lower body weight at the early stage of the experiment (week 1) and at week 8 compared with the controls (P < 0.05). No significant differences were observed at most other time points, showing a fluctuating pattern with baseline differences.ConclusionThree months of CSD led to decreased BMD and trabecular thinning in middle-aged and older male mice. No significant deterioration of overall bone biomechanical properties was observed, suggesting the presence of compensatory mechanisms in bone. The effect of sleep deprivation on body weight was intermittent rather than sustained. These findings provide experimental evidence for a comprehensive understanding of the relationship between sleep duration and skeletal health.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1809107</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1809107</link>
        <title><![CDATA[Taurine and glutamine supplementation in aging: systemic mechanisms, exercise interactions, and modulation of muscular and neurobiological pathways]]></title>
        <pubdate>2026-05-04T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Zhigang Chen</author><author>Zhiwei Niu</author>
        <description><![CDATA[The senescence of the neuro-skeletal muscle system is typified by a gradual deterioration in muscle mass, strength, neuromuscular efficacy, and cognitive capabilities, which is further exacerbated by metabolic dysregulation and heightened vulnerability to fatigue. The identification of efficacious strategies aimed at reversing or mitigating these deficits is paramount for the promotion of healthy aging. Taurine, glutamine, and physical exercise emerge as promising modulators of cellular homeostasis, exhibiting synergistic potential to address multiple pathways implicated in age-associated decline. This review amalgamates mechanistic insights into the effects of taurine and glutamine supplementation, in conjunction with exercise regimens, on protein metabolism, mitochondrial functionality, muscle fatigue biomarkers, neuroinflammation, redox equilibrium, and body composition throughout the aging process. We examine the role of taurine in preserving calcium homeostasis, enhancing mitochondrial stability, and mitigating oxidative stress; the function of glutamine in sustaining nitrogen balance, regulating immune responses, and facilitating energy metabolism; and the ability of exercise to stimulate critical signaling cascades and antioxidant networks. The integration of taurine and glutamine supplementation with systematically designed exercise regimens may yield a holistic, multi-faceted strategy for counteracting neuro–skeletal muscle aging and augmenting overall functional capacity in the elderly population.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1794324</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1794324</link>
        <title><![CDATA[Biological properties of α-actinin-2 and its role and mechanisms in disease development]]></title>
        <pubdate>2026-04-23T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Juan Meng</author><author>Shu-qiong Xu</author><author>Qi Deng</author><author>Ling-ling Jiang</author><author>Dan-Ping Huang</author><author>Qing-song Wang</author><author>Yong-Kang Wu</author>
        <description><![CDATA[α-Actinin-2 (encoded by the ACTN2 gene) is a critical cytoskeletal protein predominantly expressed in skeletal and cardiac muscle, where it anchors actin filaments to the sarcomeric Z-disk. While its structural role is well-established, emerging evidence increasingly implicates ACTN2 dysfunction in a spectrum of disorders, including cardiomyopathies, distal myopathies, and neurodegenerative conditions. Despite these established associations, a systematic synthesis of the structure-function relationship of α-Actinin-2 and its pathogenic mechanisms remains lacking. This review comprehensively summarizes the multifaceted roles of α-Actinin-2, ranging from its molecular architecture and cytoskeletal regulation to its involvement in diverse signaling pathways. Furthermore, we establish an analytical framework connecting specific genetic variants to clinical phenotypes, thereby providing theoretical insights to facilitate the identification of diagnostic biomarkers and the development of targeted therapeutic strategies.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1789642</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1789642</link>
        <title><![CDATA[Innovations in skeletal muscle regeneration: from physiology to bioengineering approaches for repair and restoration]]></title>
        <pubdate>2026-04-17T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Kamal Awad</author><author>Julia Aguirre</author><author>Misturat Adegbite</author><author>Akhilla Sajeev Kumar</author><author>Ahmed S. Yacoub</author><author>Mingxin Xia</author><author>Marco Brotto</author>
        <description><![CDATA[Skeletal muscle is a dynamic tissue essential for voluntary movement, metabolism, and thermoregulation. Yet, its intrinsic regenerative capacity is overwhelmed in volumetric muscle loss (VML), where damage exceeds the native repair threshold. Conventional treatments such as muscle flaps and grafts provide only partial structural and functional recovery, underscoring the need for regenerative strategies that more precisely recapitulate the molecular and cellular physiology of muscle healing. This review first outlines the physiology of injury and muscle regeneration, with emphasis on key molecular pathways that govern inflammation, fibrosis, and myogenesis in VML. Building on this biological framework, we then examine hydrogels as soft material platforms for skeletal muscle tissue engineering, including: (i) acellular hydrogels and nanoparticle−loaded hydrogels designed to modulate the biochemical and biophysical microenvironment; (ii) cell−loaded hydrogels that deliver myogenic or stem/progenitor cell populations; and (iii) drug−loaded hydrogels for localized, sustained release of growth factors, cytokines, nucleic acids, or small molecules. Finally, we discuss emerging directions, including nanoparticle−integrated systems, dynamically stiffening or softening hydrogels, and advanced biofabrication approaches, and consider how these cellularized and acellular drug−, cell−, or nanoparticle−loaded hydrogels can be strategically leveraged to treat complex skeletal muscle injuries.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1769763</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1769763</link>
        <title><![CDATA[Mapping the effects of exercise on cognition and physical function: a scoping review of rodent studies]]></title>
        <pubdate>2026-04-15T00:00:00Z</pubdate>
        <category>Systematic Review</category>
        <author>Muhammad Hafiz Zuhdi Fairof</author><author>Norwahidah Abdul Karim</author><author>Theng Choon Ooi</author><author>Leong Chen Lew</author><author>Arimi Fitri Mat Ludin</author><author>Nor Fadilah Rajab</author>
        <description><![CDATA[IntroductionExercise, including both resistance and aerobic modalities, is widely recognised for its cognitive and physical health benefits, such as enhanced cognitive performance, improved physical fitness, and disease prevention. An emerging field, known as chrono-exercise, examines how the timing of exercise interacts with circadian rhythms to maximise these benefits. With ageing, cognitive decline and physical impairment become increasingly prevalent, contributing to a higher risk of age-related disorders. This scoping review aims to explore whether strategies, particularly those involving brain–muscle crosstalk, can mitigate these declines.MethodThis review was conducted in accordance with PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) guidelines. Rodent studies were identified from PubMed, Scopus, Cochrane, and ProQuest databases. Included studies examined the effects of various exercise interventions, including aerobic and resistance training, on neurobehavioural outcomes, body composition, and physiological and biochemical regulatory mechanisms.ResultOverall, exercise interventions demonstrate beneficial effects on cognitive and physical health. These effects appear to be enhanced when exercise is aligned with circadian rhythms and appropriately supplemented, highlighting their potential as non-invasive strategies to mitigate age-related decline.ConclusionThese findings emphasise the need for further research to optimise exercise protocols and develop personalised interventions aimed at improving cognitive and physical health in ageing populations.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1792752</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1792752</link>
        <title><![CDATA[Exosomes in osteoporosis: regulatory mechanisms and clinical applications]]></title>
        <pubdate>2026-04-10T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Qi Shuai</author><author>Jun Tian</author><author>Wenlong Yang</author><author>Santing Huang</author>
        <description><![CDATA[Osteoporosis is a systemic metabolic bone disorder characterized by progressive bone mass reduction and microarchitectural deterioration, leading to fragility fractures. It poses a serious threat to the health of middle-aged and elderly populations and imposes a heavy healthcare burden. Exosomes mediate intercellular communication by transporting bioactive molecules such as proteins, miRNAs, and circRNAs, exerting bidirectional regulation on bone homeostasis. Exosomes derived from mesenchymal stem cells, young plasma, and plants often improve osteoporosis by promoting osteoblastic differentiation and suppressing osteoclastic activity. Conversely, exosomes originating from osteoclasts, M1 macrophages, and tumor cells tend to accelerate bone resorption. Exosomes not only provide highly specific non-invasive biomarkers for osteoporosis but also emerge as novel therapeutic carriers due to their inherent biocompatibility, targeted delivery properties, and potential for engineered modification. This systematic review examines the biological properties of exosomes, the molecular mechanisms by which exosomes from different sources regulate bone metabolism, and their application progress in the diagnosis and treatment of osteoporosis. It also explores challenges in their clinical translation, providing a comprehensive reference for further research and clinical application in this field.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1791427</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1791427</link>
        <title><![CDATA[A novel circulating osteoimmunological signature for diagnosis: integrating CXCL2, FYN, galectin-3, and STING in postmenopausal osteoporosis]]></title>
        <pubdate>2026-03-24T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Shuang Ma</author><author>Qi Yao</author><author>Xiaoxue Bao</author><author>Yukun Li</author>
        <description><![CDATA[ObjectiveThe emerging field of bone immunology has clarified the intricate interactions between the immune system and bone metabolism. This investigation was designed to examine changes in concentrations of critical immune cytokines—C-X-C motif chemokine ligand 2 (CXCL-2), FYN (a Src family nonreceptor tyrosine kinase), Galectin-3 (a β-galactoside-specific lectin), and stimulator of interferon genes (STING)—in postmenopausal osteoporotic women, and to explore their potential as biomarkers for early diagnosis of postmenopausal osteoporosis (PMOP).MethodsBetween June and September 2025, researchers recruited 100 postmenopausal women diagnosed with osteoporosis and 100 with osteopenia from the Third Hospital of Hebei Medical University, who were subsequently allocated to the Osteoporosis and Osteopenia groups, respectively. Concentrations of CXCL-2, FYN, Galectin-3, and STING were ascertained employing enzyme-linked immunosorbent assay (ELISA) across all study groups.ResultsWithin the Osteoporosis group, CXCL-2 and FYN concentrations demonstrated marked elevation relative to the NC group, whereas Galectin-3 and STING concentrations showed marked reduction (P < 0.05). Pearson correlation and multiple linear regression analyses revealed that CXCL-2, FYN, Galectin-3, and STING levels were strongly associated with BMD. ROC analysis demonstrated that Galectin-3 exhibited the greatest diagnostic precision for PMOP, with an area under the curve (AUC) of 0.881. Additionally, the combined diagnostic performance of all four factors surpassed that of any single marker.ConclusionCXCL-2, FYN, Galectin-3, and STING, as immune-related molecules, are integral to bone immune regulation and are closely associated with the pathogenesis of PMOP, positioning them as potential biomarkers for its early diagnosis.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1816216</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1816216</link>
        <title><![CDATA[Correction: Triple-gene deletion for osteocalcin significantly impairs the alignment of hydroxyapatite crystals and collagen in mice]]></title>
        <pubdate>2026-03-23T00:00:00Z</pubdate>
        <category>Correction</category>
        <author>Zihan Xu</author><author>Chao Yang</author><author>Feng Wu</author><author>Xiaowen Tan</author><author>Yaxiu Guo</author><author>Hongyu Zhang</author><author>Hailong Wang</author><author>Xiukun Sui</author><author>Zi Xu</author><author>Minbo Zhao</author><author>Siyu Jiang</author><author>Zhongquan Dai</author><author>Yinghui Li</author>
        <description></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1779440</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1779440</link>
        <title><![CDATA[Effect of distraction length on the morphology of knee cartilage in a rat model of femoral distraction osteogenesis]]></title>
        <pubdate>2026-03-16T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Caifeng Wu</author><author>Yuanxin Chen</author><author>Yanshi Liu</author><author>Lian Tang</author><author>Xiaoheng Ding</author><author>Aihemaitijiang Yusufu</author><author>Kai Liu</author>
        <description><![CDATA[ObjectiveThis study investigated the dose-dependent impact of femoral distraction length on knee joint integrity and characterized the molecular mechanisms driving cartilage degeneration in a rat distraction osteogenesis (DO) model.MethodsThirty-six Sprague-Dawley rats underwent femoral DO and were randomly assigned to three groups: Control (5 mm), Group A (10 mm), and Group B (20 mm). Following a consolidation phase, knee joint morphology and subchondral bone microstructure were evaluated using digital radiography and micro-computed tomography. Histological assessment included H&E, Safranin O-Fast Green, and Masson’s trichrome staining. Furthermore, immunohistochemical analysis quantified the expression of catabolic (IL-1β, MMP-13, RANKL) and anabolic (COL-II, SOX9, OPG) biomarkers in the articular cartilage and subchondral bone.ResultsRadiographic and histological findings demonstrated successful osseointegration and physiological tolerance in the Control and Group A. Conversely, Group B exhibited severe osteoarthritis-like pathology, including cartilage erosion, proteoglycan depletion and subchondral sclerosis. Quantitative analysis confirmed significantly elevated bone mineral density and bone volume fraction in the subchondral bone of Group B (P < 0.05). Molecularly, Group B showed significant upregulation of catabolic biomarkers (IL-1β, MMP-13 and RANKL) with concurrent downregulation of anabolic biomarkers (COL-II, SOX9 and OPG; P < 0.05).ConclusionExtensive distraction (20 mm, ∼50% of original length) surpasses the physiological adaptive capacity of the knee joint, triggering irreversible degeneration via IL-1β/MMP-13-mediated sterile inflammation and OPG/RANKL-driven osteochondral uncoupling. While moderate distraction (10 mm, ∼25% length) remains compensatory, this pathological transition highlights the critical necessity of joint protection strategies when limb lengthening targets exceed ∼25% of the original bone length.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2025.1726583</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2025.1726583</link>
        <title><![CDATA[The influence of adrenoceptor blocker treatment on fracture healing in osteoporotic and non-osteoporotic bone]]></title>
        <pubdate>2026-02-16T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Sandra Dieterich</author><author>Christoph Kölbl</author><author>Miriam Eva Angelica Tschaffon-Müller</author><author>Oliver Küppers</author><author>Dorothea Gebauer</author><author>Melanie Rebecca Kuhn</author><author>Katarina Teresa Acker</author><author>Anita Ignatius</author><author>Melanie Haffner-Luntzer</author>
        <description><![CDATA[Fracture healing is a highly dynamic process that involves inflammation, cell recruitment, angiogenesis, and subsequent bone formation and remodeling. Increasing evidence suggests the pivotal role of adrenergic signaling in musculoskeletal repair and bone-related diseases such as osteoporosis. Furthermore, impaired fracture healing in osteoporotic female mice might be attributed to an overshooting immune response with increasing numbers of neutrophils found in the early fracture hematoma. Earlier studies showed that an unspecific blockade of the β-adrenoceptor with propranolol reduces the number of neutrophils in the fracture hematoma in male mice, which might also help alleviate the overshooting immune response in female osteoporotic mice. In this study, we hypothesized that adrenoceptor blocker treatment in the early inflammatory phase of fracture healing rescues the excessive immune response in osteoporotic female mice and thereby improves fracture healing. However, our results indicate that an early blockade of adrenergic receptors does not improve fracture healing in osteoporotic and non-osteoporotic mice. In contrast to earlier studies with male mice, beta blockade (propranolol and butoxamine) in female non-osteoporotic mice increased the number of neutrophils in the early fracture hematoma, indicating an elevated immune response and a sex-dependent effect of adrenoceptor blocker treatment.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1780014</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1780014</link>
        <title><![CDATA[Reliability of DIERS pedogait system for evaluating spatiotemporal gait parameters in knee osteoarthritis and its association with Achilles tendon stiffness asymmetry]]></title>
        <pubdate>2026-02-11T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Xingxing Shen</author><author>Jiahao Chen</author><author>Jiahao Zhang</author><author>Jiaqing Tian</author><author>Sirun Cheng</author><author>Jichuan Cao</author><author>Congcong Li</author><author>Xuemeng Xu</author>
        <description><![CDATA[ObjectiveTo assess the inter-rater and test-retest reliability of DIERS pedogait system for measuring gait parameters in patients with knee osteoarthritis (KOA), and to explore inter-limb differences in Achilles tendon (AT) properties, as well as the associations between the AT stiffness asymmetry index (AsyStiffness (AT)) and gait abnormalities, visual analog scale (VAS) scores, and Kellgren-Lawrence (K/L) grades.MethodsA total of 36 patients with KOA (19 unilateral, 17 bilateral) were enrolled. Two independent assessors used DIERS pedogait system to measure gait parameters, with retesting by the first assessor 1 week later. Inter-rater and test-retest reliability were quantified using intraclass correlation coefficients (ICC), while absolute reliability was assessed using standard error of measurement (SEM), minimum detectable change (MDC), and Bland-Altman analysis. Bilateral AT muscle tone and stiffness were evaluated using the MyotonPRO. Spearman correlation and multiple linear regression analyses were performed to explore the associations of AsyStiffness (AT) with both clinical variables and gait parameters.ResultDIERS pedogait system exhibited excellent inter-rater (ICC: 0.900–0.987) and test-retest reliability (ICC: 0.927–0.988). Inter-rater SEM and MDC ranged from 0.07 to 44.26 and 0.20 to 122.68, respectively, while test-retest SEM and MDC ranged from 0.05 to 39.59 and 0.13 to 109.74. Bland-Altman analysis revealed no significant systematic bias. In addition, AT muscle tone and stiffness were significantly higher in the relatively severe leg (RSL) compared with the moderate leg (RML) (P < 0.05). AsyStiffness (AT) was positively correlated with stance phase symmetry index (ρ = 0.514, P = 0.001), stride time (ρ = 0.381, P = 0.022), VAS score (ρ = 0.373, P = 0.025), and K/L grade (ρ = 0.542, P = 0.001), and negatively correlated with gait speed (ρ = −0.374, P = 0.025). Multiple linear regression identified stance phase symmetry index (β′ = 0.298, P = 0.043), K/L grade 2 (β′ = 0.533, P = 0.017) and K/L grade 3 (β′ = 0.778, P = 0.002) as independent factors associated with AsyStiffness (AT).ConclusionDIERS pedogait system is a reliable and objective tool for assessing gait in KOA patients. AT stiffness asymmetry is associated with gait abnormalities, pain, and KOA severity. These findings suggest that early-mid interventions targeting gait abnormalities and mitigating Achilles tendon stiffness asymmetry may provide novel prophylactic and therapeutic strategies for KOA.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2025.1737373</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2025.1737373</link>
        <title><![CDATA[Meta-analysis of comparative effects of mobile app–based digital rehabilitation versus traditional rehabilitation after total knee arthroplasty]]></title>
        <pubdate>2026-01-12T00:00:00Z</pubdate>
        <category>Systematic Review</category>
        <author>Liang Ma</author><author>Jia-Qiang Liu</author><author>Kun Yu</author><author>Mei-Yun Tan</author>
        <description><![CDATA[ObjectiveThe purpose of this study is to compare the effect of digital rehabilitation based on mobile app and traditional rehabilitation program after total knee arthroplasty.MethodsThe following electronic databases were systematically searched to identify eligible trials: PubMed, EMBASE, Web of Science, the Cochrane Library, Scopus, and CINAHL. The searches were conducted from database inception to 1 December 2025. According to the inclusion and exclusion criteria, literature screening, data extraction and evaluation of its methodological quality were carried out. RevMan5.4 software was used to conduct heterogeneity test and meta-analysis of the included studies, and Cochrane systematic review tool was used to evaluate the literature publication bias. The main outcomes were visual analogue scale (VAS) of pain, “standing walking” timing test, knee function score (KSS), knee range of motion (ROM), and 10-m Walk Test.ResultsThis meta-analysis included 8 studies involving a total of 694 patients. Compared with traditional rehabilitation, the app-based group showed significantly lower pain scores, as assessed by the Visual Analogue Scale (VAS), with a positive mean difference favoring the app-based group (MD = 1.03, 95% CI 0.30 to 1.75; I2 = 0%; P = 0.006). Performance-based functional outcomes favored the app-based group, with significant improvements observed in the Timed Up and Go test (MD = −1.75, 95% CI −2.55 to −0.94; I2 = 19%; P < 0.0001) and the 10-m Walk Test (SMD = 0.47, 95% CI 0.05 to 0.88; I2 = 0%; P = 0.03). Knee range of motion (ROM) was also significantly greater in the app-based rehabilitation group (MD = 6.46°, 95% CI 2.92 to 10.00; I2 = 53%; P = 0.0004). No significant difference was observed in the Knee Society Score (KSS) between groups (P > 0.05). The overall risk of bias among the included studies was moderate, primarily due to unclear allocation concealment and lack of blinding.ConclusionCompared with traditional rehabilitation, mobile app–based digital rehabilitation after total knee arthroplasty was associated with improved pain relief and better performance-based functional outcomes, as well as greater early gains in knee range of motion. No significant difference was observed in composite knee function scores. Given the low to moderate certainty of evidence, app-based rehabilitation may be considered as an adjunct or alternative rehabilitation strategy for selected patients, while further high-quality randomized controlled trials are needed to confirm long-term effectiveness.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2025.1710819</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2025.1710819</link>
        <title><![CDATA[Comparison of quadriceps femoris properties, surface electromyography parameters and foot posture asymmetries between patients with unilateral and bilateral knee osteoarthritis]]></title>
        <pubdate>2025-12-02T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Xingxing Shen</author><author>Jiaqing Tian</author><author>Jiahao Chen</author><author>Jiahao Zhang</author><author>Sirun Cheng</author><author>Ruian Xiang</author><author>Xuemeng Xu</author>
        <description><![CDATA[ObjectiveTo investigate the differences in quadriceps femoris (QF) properties, surface electromyography (sEMG) parameters and foot posture asymmetries between patients with unilateral and bilateral knee osteoarthritis (KOA), and to analyze the factors related to foot posture asymmetry.MethodsA total of 32 patients with unilateral KOA (unilateral group, UG) and 35 patients with bilateral KOA (bilateral group, BG) were enrolled in this study. The severity of knee osteoarthritis symptoms was assessed, and the affected legs were categorized as relatively severe leg (RSL) or relatively moderate leg (RML) based on the Visual Analogue Scale (VAS). Surface electromyography was utilized to measure the root mean square (RMS) values of rectus femoris (RF), vastus medialis (VM), and vastus lateralis (VL) during a straight leg raise task. Biomechanical characteristics, including muscle tone and stiffness, were measured using MyotonPRO. The foot posture index-6 (FPI-6) was applied to assess foot posture and asymmetrical foot posture scores. Additionally, we calculated the asymmetry indices of muscle tone (AsyTone), stiffness (AsyStiffness), and root mean square (AsyRMS) for the QF, along with their FPI asymmetry scores.ResultIn the evaluation of RF, VM, and VL in both groups, the RMS on the RML was significantly higher than that on the RSL (P < 0.05), while muscle tone and stiffness on the RSL were significantly higher than those of the RML (P < 0.05). In UG, AsyTone (RF), AsyTone (VM), AsyStiffness (RF), AsyStiffness (VM), AsyStiffness (VL) and AsyRMS (VM) were significantly higher than those in BG (P < 0.05). AsyTone (VL) was significantly lower than that in BG (P < 0.01). There was no significant difference in AsyRMS (RF) and AsyRMS (VL) between the two groups (P > 0.05). Regarding the FPI asymmetry scores, the proportion of asymmetry (including asymmetry and severe asymmetry) in the UG (65.6%) was much more frequent compared with that of BG (34.3%), with a statistically significant difference (χ2 = 6.57, P = 0.01). Furthermore, the VAS score and K/L grade were significantly correlated with the FPI asymmetric score in the UG (b = 1.065; 95% CI: 0.194, 1.936; p = 0.019 and b = 1.770; 95% CI: 0.215, 3.325; p = 0.028, respectively) and BG (b = 0.665; 95% CI: 0.117, 1.212; p = 0.020 and b = 1.523; 95% CI: 0.414, 2.632; p = 0.009, respectively).ConclusionBoth unilateral and bilateral patients with KOA exhibited a propensity for asymmetry in the properties of the QF, RMS values, and foot postures on both sides. Notably, unilateral patients tended to demonstrate this asymmetry more prominently and exhibit a higher prevalence of foot posture asymmetry compared to those bilateral patients. Furthermore, the degree of foot posture asymmetry was closely linked to pain severity and K/L grading whether in unilateral or bilateral KOA patients.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2025.1717233</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2025.1717233</link>
        <title><![CDATA[The role of cell death in the physiological and pathological processes of skeletal muscle]]></title>
        <pubdate>2025-11-17T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Hongyi Xu</author><author>Zihui Gao</author><author>Xinlei Yao</author><author>Jiacheng Sun</author><author>Bingqian Chen</author>
        <description><![CDATA[Skeletal muscle is the largest metabolic and motor organ in the human body. It facilitates daily movement and maintains posture through contraction. It also acts as a core tissue for energy metabolism by participating in glucose uptake, lipid oxidation, and thermogenesis. Thus, it plays a vital role in regulating systemic metabolic homeostasis. Under physiological conditions, skeletal muscle maintains a dynamic regulatory network to coordinate multiple cellular processes for tissue homeostasis. Apoptosis selectively removes damaged myonuclei and maintains myofiber structural integrity. Necroptosis prevents excessive inflammatory responses. Autophagy degrades abnormal proteins and organelles to ensure cytoplasmic quality control. Additionally, pyroptosis supports immune surveillance. In pathological states, abnormal activation of cell death programs occurs. These include apoptosis, necrosis, autophagy, pyroptosis, and ferroptosis. Such dysregulation can lead to myonuclear loss, myofiber atrophy, and fibrosis. While previous reviews have often focused on individual cell death pathways, this review provides a novel, integrated perspective by systematically outlining the roles and regulatory mechanisms of multiple death modalities in skeletal muscle. The interactions and balances among these pathways collectively determine muscle fate. We further discuss the implications of this network across various pathological contexts, such as muscular dystrophy, sarcopenia, and sepsis-induced atrophy. Finally, we identify promising therapeutic targets arising from this integrated view and discuss the challenges and future directions for translating these findings into clinical strategies. This review provides a comprehensive theoretical foundation for understanding the pathogenesis and treatment of skeletal muscle-related diseases.]]></description>
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        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2025.1664568</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2025.1664568</link>
        <title><![CDATA[Multiple pathways of the actin-myosin cycle in energy transduction and the release of orthophosphate in muscle]]></title>
        <pubdate>2025-11-04T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Marco Caremani</author><author>Irene Pertici</author><author>Ilaria Morotti</author><author>Pasquale Bianco</author><author>Massimo Reconditi</author><author>Gabriella Piazzesi</author><author>Vincenzo Lombardi</author><author>Marco Linari</author>
        <description><![CDATA[In the striated muscle, the molecular motor myosin II functions in two bipolar arrays in each thick filament, converting chemical energy into steady force and shortening by cyclic ATP-driven interactions with nearby actin filaments. The fundamental steps in energy transduction are the working stroke, an inter-domain tilting of the lever arm about the actin-attached catalytic domain, generating up to ∼5 pN force or ∼10 nm of filament sliding, and the release of the ATP hydrolysis product orthophosphate (Pi) from the nucleotide-binding site, which is associated with a large free energy release. The two events are not simultaneous, as first demonstrated by the force response to a stepwise change in [Pi] (the Pi transient), showing the saturation kinetics characteristic of a two-step reaction. However, while high-resolution crystal structures of the myosin motor suggest that Pi release precedes the working stroke, in vitro functional studies indicate that it follows the working stroke. High-resolution sarcomere-level mechanics applied to single muscle fibers, allowing myosin motor synchronization by step perturbations in length or load, revealed that the kinetics of the working stroke is independent of [Pi] and depends only on the load. Moreover, this approach highlights the need for two unconventional pathways of the chemo-mechanical cycle: an early detachment of the force-generating motors and the possibility for attached motors to slip to the next actin monomer farther from the sarcomere center during shortening. Transient and steady-state responses to stepwise changes in load or [Pi] can be fitted with a structurally and biochemically explicit model in which the Pi release step is orthogonal to the progression of the working stroke. Model simulations indicate that the rate of Pi release depends on motor conformation, which resolves longstanding unanswered questions such as the dependence of Pi transient kinetics on the final level of [Pi] under any load and clarifies the issue of the relative timing between the working stroke and Pi release: at high loads, Pi release precedes the execution of the working stroke, while at low loads, the working stroke state transitions are fast enough to occur with Pi still bound to the catalytic site.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2025.1684102</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2025.1684102</link>
        <title><![CDATA[Non-neuronal cholinergic stimulation favors bone mass accrual]]></title>
        <pubdate>2025-11-03T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Faleh Tamimi</author><author>Hazem Eimar</author><author>Sharifa Alebrahim</author><author>Lina Abu-Nada</author><author>Garthiga Manickam</author><author>Ahmed Ebraheem Al Subaie</author><author>Iskandar Tamimi</author><author>Monzur Murshed</author>
        <description><![CDATA[IntroductionNon-neuronal cholinergic receptors are expressed in immune cells and their stimulation has been shown to regulate the secretion of several cytokines. Some of these cytokines, such as interleukin-17 (IL-17), IL-23, interferon-γ (IFN-γ) and tumor necrosis factor-α (TNF-α), are known to regulate bone mass. Accordingly, we hypothesize that stimulating cholinergic receptors in non-neuronal cells, such as immune cells, promotes bone mass accrual.MethodsTo test this hypothesis, we used neostigmine, a drug that increases acetylcholine levels by inhibiting acetylcholinesterase activity in peripheral tissues. Female C57BL/6 mice were treated with neostigmine for six weeks, and μCT, histomorphometry, Raman spectroscopy, X-ray diffraction, and mechanical testing were used to analyze bone parameters. A rat model was used to assess bone defect healing and implant osseointegration. Serum cytokines were measured by ELISA, and IL-17 effects on osteoblast proliferation were evaluated in vitro.ResultsHere, we show that 6 weeks of neostigmine treatment promotes bone mass accrual in endochondral bones of both the axial and appendicular skeleton in mice. Moreover, the administration of neostigmine for 2 weeks accelerated the healing process of the surgically induced bone defects in rats. The body mass index, body weight, visceral fat pad weight and epinephrine levels in the neostigmine-treated mice were similar to those of saline-treated mice, indicating that neostigmine favored bone mass accrual by acting peripherally rather than centrally. The increased bone mass in the neostigmine-treated mice was caused by an increase in osteoblast proliferation and bone formation rate. We also observed an increase in circulating immunocytokine IL-17 levels in the neostigmine-treated mice. Statistical analysis showed that the increase in serum IL-17 level was associated with the increase in osteoblast number. In agreement with our findings from the in vivo experiments, IL-17 treatment increased the proliferation of MC3T3.E1 preosteoblasts in vitro, while acetylcholine or neostigmine did not have any significant effect. ConclusionTaken together, our findings indicate that peripheral cholinergic stimulation promotes bone mass accrual, in part through IL-17–mediated osteoblast activity. Although the evidence is correlative, these results highlight a potential neuro-immune pathway and suggest new therapeutic directions for enhancing bone formation and regeneration.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2025.1711795</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2025.1711795</link>
        <title><![CDATA[Meeting report: the inaugural muscle biology and cachexia conference at the University of Houston, May 18-20, 2025, Houston, Texas, USA]]></title>
        <pubdate>2025-10-30T00:00:00Z</pubdate>
        <category>Perspective</category>
        <author>Jingjuan Chen</author><author>Marco Brotto</author><author>Radbod Darabi</author><author>Ashok Kumar</author>
        <description><![CDATA[In May 2025, the University of Houston (UH) hosted the inaugural Muscle Biology and Cachexia conference, organized by Drs. Ashok Kumar and Radbod Darabi. The conference attracted nearly 300 participants, including established scientists, early-career researchers, and students from across the United States, Canada, Italy, Singapore, and Turkey. Research was presented through a combination of oral presentations and poster sessions. The conference was driven by the increasing interest in skeletal and cardiac muscle biology and cancer cachexia among institutions at the Texas Medical Center and surrounding universities. It served as a platform to promote knowledge exchange and foster collaboration within this growing scientific community. The conference was supported by the UH College of Pharmacy (UHCOP), Division of Research (DOR), Drug Discovery Institute (DDI), and the Department of Pharmacological and Pharmaceutical Sciences (PPS). In conjunction with the conference, UH announced the formation of the Institute of Muscle Biology and Cachexia (IMBC). The IMBC aims to strengthen collaborative research efforts and enhance understanding of the molecular and signaling pathways that regulate muscle physiology and disease.]]></description>
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        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2025.1685955</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2025.1685955</link>
        <title><![CDATA[Single-cell sequencing reveals cellular heterogeneity and molecular mechanisms in tendon and enthesis injury repair]]></title>
        <pubdate>2025-10-29T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Tingming Pan</author><author>Zhong Dong</author><author>Hongjie Zhang</author><author>Fengmin Yang</author><author>Yating Chen</author>
        <description><![CDATA[BackgroundTendon and enthesis injuries represent a significant global health challenge, severely impairing patient mobility and self-care abilities while imposing substantial medical burdens.Main BodyPoor clinical outcomes in tendon healing stem from the complex enthesis, which involves diverse cell types and signaling pathways. Recent advances in single-cell sequencing technologies have revealed detailed cellular diversity and function in tendon and tendon-bone healing. Using multimodal integration, researchers have identified precise subpopulations of tendon and enthesis cells. They have also clarified cell-to-cell crosstalk and mapped differentiation paths during healing.ConclusionThese new findings, guided by emerging methodological advancements. They offer innovative perspectives for developing targeted clinical interventions for tendon and enthesis injury.]]></description>
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