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        <title>Frontiers in Physiology | Mitochondrial Research section | New and Recent Articles</title>
        <link>https://www.frontiersin.org/journals/physiology/sections/mitochondrial-research</link>
        <description>RSS Feed for Mitochondrial Research section in the Frontiers in Physiology journal | New and Recent Articles</description>
        <language>en-us</language>
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        <pubDate>2026-05-14T09:59:29.423+00:00</pubDate>
        <ttl>60</ttl>
        <item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1797296</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1797296</link>
        <title><![CDATA[Mitochondria-associated membranes in heart failure: from molecular mechanisms to therapeutic targets]]></title>
        <pubdate>2026-05-12T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Shuning Li</author><author>Yanjie Lian</author><author>Xiaolei Lai</author><author>Juju Shang</author><author>Wenlong Xing</author><author>Hongxu Liu</author>
        <description><![CDATA[Mitochondria-associated endoplasmic reticulum membranes (MAMs) serve as pivotal functional contact sites linking mitochondria and the endoplasmic reticulum, playing a role in orchestrating various cellular life activities, including calcium homeostasis, mitochondrial quality control, endoplasmic reticulum stress, lipid synthesis and transport, inflammation and innate immunity, apoptosis, autophagy, ferroptosis, and oxidative stress. Recent research has demonstrated that the structural and functional dysregulation of MAMs significantly contributes to the onset and progression of heart failure. This review systematically examined the molecular composition, structural features, and dynamic regulatory mechanisms of MAMs, emphasizing their central roles in the pathophysiological processes of heart failure, such as calcium homeostasis imbalance, mitochondrial dynamics disorders, endoplasmic reticulum stress, metabolic reprogramming, and inflammatory and immune responses. We proposed an in-depth analysis of the differential manifestations of MAMs across distinct heart failure phenotypes (HFrEF and HFpEF) and summarized potential therapeutic strategies targeting MAMs, along with the challenges encountered in their clinical translation. Finally, we proposed a novel research paradigm for MAMs based on multi-omics integration and artificial intelligence, offering a theoretical foundation for the development of precise treatment plans for heart failure.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1782863</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1782863</link>
        <title><![CDATA[Mitophagy in kidney and lung epithelial cells: molecular mechanisms, crosstalk, and therapeutic interventions]]></title>
        <pubdate>2026-05-12T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Xiaoxi Zhou</author><author>Jing Sun</author><author>Lining Miao</author><author>Yixian Zhang</author>
        <description><![CDATA[Mitophagy is a central component of mitochondrial quality control in both renal tubular and alveolar epithelial cells, where mitochondrial homeostasis is essential for barrier integrity, energy supply, and stress adaptation. Increasing evidence indicates that mitophagy is highly context-dependent across kidney and lung diseases: insufficient mitochondrial clearance is commonly linked to persistent mitochondrial dysfunction, epithelial senescence, and fibrotic remodeling, whereas dysregulated or excessive mitophagy may aggravate epithelial vulnerability under severe inflammatory or infectious stress. In this review, we summarize the molecular regulation of epithelial mitophagy, including PINK1/Parkin-dependent and receptor-mediated pathways, and examine its divergent roles in acute and chronic injury states in the kidney and lung. We further discuss a proposed mitophagy-centered framework for kidney–lung crosstalk. Current evidence is strongest for kidney-to-lung communication, particularly through circulating mitochondrial damage-associated molecular patterns and inflammatory mediators after acute kidney injury, whereas lung-to-kidney links remain supported mainly by organ-level inflammatory, hypoxemic, and hemodynamic mechanisms rather than direct evidence of pulmonary epithelial mitophagy-driven renal injury. Overall, the available literature supports mitophagy as an important mechanistic interface in epithelial injury, but not yet as a fully validated bidirectional epithelial axis. Future therapeutic strategies should therefore aim to restore mitophagy homeostasis in a disease- and stage-specific manner rather than uniformly enhancing or suppressing mitochondrial clearance.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1716764</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1716764</link>
        <title><![CDATA[Direct dapagliflozin exposure enhances respiration and membrane hyperpolarization in isolated cardiac mitochondria]]></title>
        <pubdate>2026-05-01T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Itanna Isis Araújo de Souza</author><author>César Francisco Maricato da Rosa</author><author>Laís Eduardo Marinho</author><author>Marcella Borges Coutinho</author><author>Caroline Da Silva Moraes</author><author>Antonio Carlos Campos de Carvalho</author><author>José Hamilton Matheus Nascimento</author><author>Leonardo Maciel de Oliveira Pinto</author>
        <description><![CDATA[Dapagliflozin, a sodium–glucose cotransporter 2 (SGLT2) inhibitor widely used for the treatment of diabetes, has been consistently associated with cardiovascular protection, including attenuation of ischemia/reperfusion injury and reduced incidence of heart failure. However, the cellular and molecular mechanisms underlying these effects remain incompletely understood. In this context, the present study aimed to investigate whether dapagliflozin exerts direct effects on mitochondrial function and bioenergetics. Cardiac mitochondria were isolated from Wistar rats (Rattus norvegicus), and mitochondrial function was systematically evaluated by assessing oxygen consumption, ATP production, reactive oxygen species (ROS) generation, and mitochondrial membrane potential following exposure to dapagliflozin (10 nM). Dapagliflozin increased oxygen consumption in states 1–3 supported by complex I substrates and enhanced both basal and ADP-stimulated respiration in complex II, without affecting state 4 respiration, complex IV activity, or maximal uncoupled respiration. In parallel, dapagliflozin significantly reduced mitochondrial ROS production in both complexes I and II without altering ATP generation, resulting in an increased ATP/ROS ratio, indicative of improved bioenergetic efficiency. Notably, electron leakage was increased in complex I but remained unchanged in complex II, suggesting differential modulation of electron transport chain components. Furthermore, dapagliflozin induced mitochondrial membrane hyperpolarization in the presence of Ca2+, with or without oligomycin, and to a lesser extent in the presence of K⁺, while no significant effects were observed under Na⁺ conditions. Collectively, these findings demonstrate that dapagliflozin directly modulates mitochondrial bioenergetics and redox balance, supporting a mechanistic link between mitochondrial function and its cardioprotective effects.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1721230</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1721230</link>
        <title><![CDATA[Mitochondrial metabolic reprogramming, quality control, and intercellular transfer in regulating macrophage plasticity]]></title>
        <pubdate>2026-05-01T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Guanheng He</author><author>Qian Sun</author>
        <description><![CDATA[Macrophage functional plasticity is intrinsically linked to metabolic reprogramming, including mitochondrial function, substrate utilization, and redox signaling. In response to hypoxia, infection, or tissue injury, macrophages rely on mitochondria not only for energy provision but, critically, for metabolic intermediates and reactive oxygen species (ROS) that serve as signaling molecules to guide gene expression reprogramming. While macrophage activation exists along a continuous spectrum, this review summarizes the distinct metabolic paradigms characterizing the classical M1-like (glycolysis-dominant) and M2-like (oxidative phosphorylation, OXPHOS-dominant) extremes, highlighting the molecular mechanisms where metabolic events—specifically tricarboxylic acid (TCA) cycle truncation and succinate accumulation—drive inflammatory polarization. Furthermore, we discuss the role of mitochondrial quality control, particularly dynamics and mitophagy, in maintaining macrophage homeostasis. Notably, recent evidence identifies “intercellular mitochondrial transfer” as a novel mode of immune microenvironment regulation, enabling damaged macrophages to restore function by acquiring exogenous mitochondria. A deeper understanding of these mechanisms offers new intervention targets for metabolic immunotherapy in sepsis, cancer, and chronic inflammatory diseases. Importantly, we emphasize that many of these metabolic and mitochondrial regulatory mechanisms are highly context-dependent, varying significantly across different tissues and disease microenvironments.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1826699</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1826699</link>
        <title><![CDATA[GLP-1 receptor and Mitochondria-ER Contact Sites: an emerging mechanism of metabolic regulation]]></title>
        <pubdate>2026-04-28T00:00:00Z</pubdate>
        <category>Mini Review</category>
        <author>Pablo Cruz</author><author>Andrea Puebla-Huerta</author><author>Mayarling F. Troncoso</author><author>Eduardo Silva-Pavez</author><author>Yessia Hidalgo-Fadic</author><author>Ulises Ahumada-Castro</author>
        <description><![CDATA[The uncoupling of Mitochondria-ER Contact Sites (MERCS) represents a hallmark of metabolic dysfunction in obesity and type 2 diabetes. These are dynamic interfaces that play essential roles in coordinating ion signaling and lipid exchange to maintain cellular homeostasis. Persistent organelle stress in chronic disease impairs these pathways, driving systemic hormone resistance and metabolic failure. A paradigm shifts in glucagon-like peptide-1 receptor (GLP-1R) signaling from diffuse events to spatiotemporally organized signalosomes offer insightful mechanisms into these conditions. The localization of internalized GLP-1Rs at the Mitochondria-ER interface supports a contactomics framework for understanding bioenergetic restoration. Stabilizing inter-organellar connectivity represents a novel frontier for next-generation metabolic therapies.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1840059</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1840059</link>
        <title><![CDATA[Editorial: Mechanisms and novel therapeutic targets and approaches for mitochondrial dysfunction in neurological and cardiovascular diseases]]></title>
        <pubdate>2026-04-21T00:00:00Z</pubdate>
        <category>Editorial</category>
        <author>Qiuxia Li</author><author>Quanjiang Zhang</author>
        <description></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1735677</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1735677</link>
        <title><![CDATA[Quantitative reconstruction of neuronal mitochondrial network in neurites and somata in rat hippocampus and prefrontal cortex]]></title>
        <pubdate>2026-04-21T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Lu Wang</author><author>Linlin Li</author><author>Jiazheng Liu</author><author>Zichen Wang</author><author>Jing Liu</author><author>Sheng Chang</author><author>Jingbin Yuan</author><author>Xi Chen</author><author>Qiwei Xie</author><author>Lijun Shen</author><author>Xianhua Wang</author><author>Gang Li</author><author>Heping Cheng</author><author>Hua Han</author>
        <description><![CDATA[IntroductionMitochondrial networks exhibit striking heterogeneity in their morphology and distribution across different neuronal compartments, reflecting the diverse metabolic demands of these structures.MethodsIn this study, we used automated tape-collecting ultramicrotome scanning electron microscopy (ATUM-SEM) to reconstruct and quantify mitochondrial networks in the somata and neurites of neurons in the rat prefrontal cortex (PFC) and hippocampus (HPC; CA1 stratum radiatum). We developed an automated segmentation pipeline based on an attention-enhanced 3D U-Net to extract all mitochondria from volumetric EM data.ResultsOur quantitative analyses revealed pronounced regional and subcellular heterogeneity. In the PFC, the mitochondrial volume fraction was higher in neurites (7.2%) than in somata (2.9%; 7.1% when nucleus was excluded). Mean individual mitochondrial volume was 0.11 μm³ for neuritic and 0.33 μm³ for somatic mitochondria in the PFC, with similar results observed in the HPC (0.13 μm³ in neurites, 0.31 μm³ in somata). In both regions, the vast majority of mitochondria (~91%) assumed an oval or rod shape, with few displaying branched or donut-shaped structures (~1%). Notably, elongated linear mitochondria (~8%) were mostly confined to neurites, and approximately 90% of these comprised up to 120 nanotunnels—thin segments (<220 nm) connecting enlarged, oval-shaped structures (>350 nm) in tandem.ConclusionThese data provide a detailed quantitative characterization of mitochondrial network architecture in the adult rat cortex and hippocampus, revealing significant regional and subcellular differences in mitochondrial morphology and distribution.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1782998</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1782998</link>
        <title><![CDATA[Investigation of mitochondrial inner membrane ion conductance by planar lipid bilayer electrophysiology]]></title>
        <pubdate>2026-04-20T00:00:00Z</pubdate>
        <category>Methods</category>
        <author>Amrendra Kumar</author><author>Eleanora Margulis</author><author>Nelli Mnatsakanyan</author>
        <description><![CDATA[Mitochondrial ion channels are proteins of the inner and outer mitochondrial membranes that regulate ion flux and control various cellular processes, including calcium signaling, bioenergetic and metabolic functions, and cell death. Their precise regulation is essential to maintaining normal mitochondrial function and preventing pathological processes. Patch-clamp and planar lipid bilayer electrophysiology techniques have been used to measure ion flow directly across the membrane, thereby revealing the gating kinetics and pharmacological profile of ion channels in real time. Here, we describe a planar lipid bilayer electrophysiology approach for assessing mitochondrial ion channel conductance using mitochondrial inner membrane vesicles (IMVs). The comparative electrophysiology analysis between IMVs and purified mitochondrial proteins, ATP synthase, and the adenine nucleotide translocator (ANT), demonstrates that planar lipid bilayer electrophysiology is a robust tool for biophysical characterization of mitochondrial ion channels using IMVs. This approach is particularly valuable for investigating ion channel properties under controlled yet physiologically relevant conditions and for evaluating the direct modulatory effects of different pharmacological agents.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1798354</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1798354</link>
        <title><![CDATA[Remote stimulation of mitochondria and the antioxidant potential of thymocytes by weak non-ionizing non-thermal broadband pulsed electromagnetic fields in mouse]]></title>
        <pubdate>2026-04-16T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Denis Viktorovich Ivanov</author><author>Elena Vladimirovna Bondarchuk</author><author>Igor Feodorovich Turkanov</author><author>Irina Victorovna Kuzmina</author><author>Grigory Arnoldovich Flaks</author><author>Ekaterina A. Galkina</author><author>Valery Gryaznov</author>
        <description><![CDATA[Leading medical centers are currently considering pulsed electromagnetic therapy as a promising approach to prolong active life.ObjectiveThe aim of this study was to investigate the effects of non-ionizing electromagnetic fields on mitochondrial activity and the state of the lipid peroxidation system, an antioxidant protection system in mice.MethodologyThe studies were carried out on 60 BALB/c mice in accordance with bioethical standards and general ethical principles of animal experimentation. The animals were divided into 5 groups. The groups were placed in different rooms, standing at a considerable distance from each other. Experimental animals were exposed to non-invasive electromagnetic therapy device “TOR”. The mitochondrial activity of thymocytes and the total antioxidant potential of the blood plasma were analyzed in all animals.ResultsThe study showed that weak non-ionizing non-thermal broadband pulsed electromagnetic fields (EMF) increased the antioxidant potential of mouse blood: at minimum exposure (1 min/h/10 nights) by almost 8% (p > 0.05), at maximum (5 min/h/10 nights) - by 20.6% (p< 0.05) - compared to the negative control group (young animals not exposed to EMF). The experiment confirms the dose-dependent stimulating effect of EMF on the mitochondria of thymocytes; at maximum exposure, the changes become statistically significant (increase in mitochondrial fluorescence by 29% compared to the negative control group, p< 0.05).ConclusionThe biological effects of non-ionizing electromagnetic fields are diverse. Due to their high penetrating power, they are able to affect deep-seated organs and tissues, thereby opening up new approaches in medicine and regenerative therapy that are cost-effective for patients and elicit cellular responses similar to physical exercise.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1829446</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1829446</link>
        <title><![CDATA[Editorial: Mitochondrial dynamics and endothelial dysfunction: implications for metabolic disorders]]></title>
        <pubdate>2026-03-27T00:00:00Z</pubdate>
        <category>Editorial</category>
        <author>Dorota Dymkowska</author><author>Aneta Balcerczyk</author>
        <description></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1774714</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1774714</link>
        <title><![CDATA[Recalibrating cell fate: targeting the mitochondrial signaling hub with natural active compounds to inhibit regulated cell death in diabetic kidney disease]]></title>
        <pubdate>2026-03-23T00:00:00Z</pubdate>
        <category>Mini Review</category>
        <author>Yinzhong Dai</author><author>Chenguang Wu</author><author>Jiaying Zheng</author><author>Keqin Zhao</author><author>Shimei Hua</author><author>Jianing Sun</author><author>Han Zhu</author><author>Jun Luo</author><author>Junwei Shi</author><author>Lu Han</author><author>Lifan Wang</author><author>Peng Liu</author>
        <description><![CDATA[Diabetic kidney disease (DKD) is the leading cause of end-stage renal disease worldwide. The progression of DKD is closely related to various cell death (RCD) pathways such as apoptosis, pyroptosis and ferroptosis. Although historically viewed as distinct events, we propose that mitochondria function as the central hub integrating hyperglycemic, lipotoxic, and pro-inflammatory insults. We delineate how initial hyperglycemic and hemodynamic insults compromise mitochondrial quality control, triggering a vicious cycle: dysfunctional mitochondria release ROS and damage-associated molecular patterns to initiate regulated cell death and inflammation, which in turn further impairs mitochondrial bioenergetics, thereby amplifying diabetic kidney injury. Mechanistically, mitochondrial outer membrane permeabilization triggers intrinsic apoptosis, while the cytosolic leakage of mitochondrial reactive oxygen species (mtROS) and mitochondrial DNA (mtDNA) primes the NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome to drive pyroptosis. In parallel, organelle-level metabolic and redox instabilities fuel the lipid peroxidation characteristic of ferroptosis. We highlight the sophisticated crosstalk within this network, such as the Caspase-3/Gasdermin E switch, arguing that these pathways function as a network of molecular crosstalk and functional interdependence with distinct spatiotemporal dynamics, rather than a singular execution program. Regarding therapeutic interventions, we summarize preclinical evidence for natural active compounds like berberine and quercetin. These phytochemicals act as network-level modulators of mitochondrial targets to restore cellular homeostasis. Finally, we critically address the “translational gap” posed by poor oral bioavailability and lack of human target validation. We also explore emerging biophysical concepts, such as liquid-liquid phase separation, as a speculative yet novel frontier for organizing pathological metabolic signals. Therefore, disrupting this mitochondrial feedback loop, when coupled with advanced delivery strategies, represents a strategic therapeutic avenue to arrest DKD progression.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1777143</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1777143</link>
        <title><![CDATA[The interaction between sarcoplasmic reticulum and mitochondria: a novel mechanism for cardiac arrhythmia]]></title>
        <pubdate>2026-03-16T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Zhongyang Yu</author><author>Meng Zhao</author><author>Hongyue Xu</author><author>Ji Sun</author><author>Xiaoxing Jin</author>
        <description><![CDATA[Cardiovascular diseases are a major cause of morbidity and mortality worldwide. Cardiac arrhythmias, especially fatal ventricular arrhythmias, are highly harmful to patients and can even lead to sudden death. While electrical and structural remodeling of myocardial tissue represent the mainstream mechanisms underlying arrhythmogenesis, there is a critical need to explore novel perspectives. This review focuses on the communication between the sarcoplasmic reticulum and mitochondria as an independent mechanistic lens. We detail how this specific interaction governs Ca2+ transfer and cell-death signaling, positioning it as a potentially pivotal, distinct pathway that contributes to and amplifies the development of cardiac arrhythmias.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1783596</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1783596</link>
        <title><![CDATA[Mitochondrial ROS dyshomeostasis: a key driver of accelerated supraspinatus atrophy after rotator cuff injury]]></title>
        <pubdate>2026-03-12T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Erkai Pang</author><author>Yijin Zou</author><author>Kongye Lu</author><author>Jian Li</author><author>Xuxu Chen</author><author>Yu Zhu</author><author>Tao Wang</author><author>Linlin Shi</author><author>Hui Kang</author>
        <description><![CDATA[Rotator cuff injuries are common musculoskeletal disorders and are frequently accompanied by progressive supraspinatus muscle atrophy, which severely compromises functional recovery and surgical outcomes. Accumulating evidence indicates that mitochondrial reactive oxygen species (mtROS) dyshomeostasis is a central pathological driver of post-injury muscle degeneration. This review synthesizes current knowledge on the anatomical and histopathological changes following rotator cuff tears and focuses on the mechanisms governing mitochondrial ROS production, clearance, and dysregulation in the supraspinatus muscle. We highlight how excessive mtROS contribute to oxidative damage, mitochondrial dysfunction, impaired energy metabolism, and activation of key atrophy-related signaling pathways, including FOXO, NF-κB, MAPK, the ubiquitin-proteasome system, and the autophagy-lysosome pathway. Particular emphasis is placed on the unique biomechanical unloading, ischemic stress, and metabolic vulnerability of the supraspinatus following rotator cuff injury, which predispose this muscle to ROS-driven degeneration. Finally, we critically evaluate emerging therapeutic strategies targeting mtROS, including mitochondria-targeted antioxidants and conventional redox-modulating interventions, and discuss their translational potential and current limitations.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1759575</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1759575</link>
        <title><![CDATA[PANoptosis and mitochondrial regulatory mechanisms in cerebral ischemia-reperfusion injury]]></title>
        <pubdate>2026-03-06T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Li Li</author><author>Chunyan Guo</author><author>Zheng Zuo</author><author>Luoyang Cai</author><author>Xin Chen</author><author>Yongjiang Fang</author><author>Shengnan Zhang</author><author>Tianyu Chen</author><author>Peng Kuang</author><author>Pengyue Zhang</author><author>Li Li</author><author>Zuhong Wang</author>
        <description><![CDATA[Cerebral ischemia-reperfusion injury remains a leading cause of mortality and disability despite advances in reperfusion therapy. Traditional research has focused on individual cell death pathways, yet pharmacological blockade of single pathways provides only partial neuroprotection, suggesting that dying cells engage multiple death routes simultaneously. This review examines whether PANoptosis, an inflammatory cell death modality characterized by concurrent activation of apoptotic, necroptotic, and pyroptotic pathways, occurs in cerebral ischemia-reperfusion injury. The analysis demonstrates that mitochondrial dysfunction serves as the central convergence point orchestrating multi-pathway death activation across distinct temporal phases. Ischemia creates metabolic crisis that primes mitochondria without triggering irreversible commitment. Reperfusion causes explosive mitochondrial collapse through oxidative stress, releasing danger signals that simultaneously engage multiple death pathways. Impaired mitochondrial quality control then sustains inflammatory amplification over extended periods. Multiple lines of evidence support this framework, including concurrent rather than sequential appearance of pathway markers, mixed morphological features within individual cells, pathway redundancy demonstrated by incomplete single-target protection, and mechanistic convergence at the mitochondrial level. Cellular responses vary among neurons, astrocytes, microglia, and endothelial cells but share the common feature of coordinated multi-pathway activation. This integrated understanding explains why single-pathway therapeutic approaches have failed clinically and suggests that effective neuroprotection requires targeting upstream mitochondrial dysfunction or addressing pathway redundancy through multi-target interventions.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1767822</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1767822</link>
        <title><![CDATA[Research trends of mitochondrial dysfunction in hepatic fibrosis: a bibliometric analysis]]></title>
        <pubdate>2026-02-27T00:00:00Z</pubdate>
        <category>Systematic Review</category>
        <author>Xingtao Jin</author><author>Yanlu Ma</author><author>Yiqiang Tang</author><author>Fengjie Qiao</author><author>Tong Xiao</author><author>Yu Cui</author><author>Man Li</author><author>Yueqiu Gao</author>
        <description><![CDATA[BackgroundHepatic fibrosis is a progressive pathological process driven by multiple chronic liver injury factors. Increasing evidence highlights that mitochondrial dysfunction serves as a pivotal mechanism in the onset and progression of hepatic fibrosis.MethodsA systematic search of the Web of Science Core Collection (WoSCC) and Scopus databases identified 1,634 relevant articles published between January 2005 and December 2025. Following the PRISMA guidelines, duplicate removal and quality control were performed. Bibliometric analysis tools including VOSviewer, CiteSpace, and Scimago Graphica were utilized to extract or calculate evaluation metrics, enabling analysis and visualization of knowledge maps. Publications were categorized by country, institution, author, journal, highly cited papers, and keywords. These variables were compared in terms of publication output and academic impact, including metrics such as citation counts, citation impact, H-index, and journal impact factor.ResultsA total of 1,634 relevant publications were retrieved, originating from 92 countries or regions and 2858 research institutions. China and the United States led in both publication volume and impact; the most prolific institution was the Centro de Investigación Biomédica en Red (CIBER), followed by the University of California System. The International Journal of Molecular Sciences was the most frequently publishing journal, while Hepatology was the most highly cited journal. Heidari, Reza was the most prolific author; the five most cutting-edge keywords identified were oxidative stress, apoptosis, mitophagy, hepatic stellate cells, and reactive oxygen species. We confirmed three major research hotspots: activation of hepatic stellate cells, imbalance in mitochondrial quality control, and the vicious cycle of oxidative stress.ConclusionBased on our previous discussions, mitochondria are increasingly recognized as central to the onset and progression of hepatic fibrosis. Related research is advancing rapidly and has become a key area for interdisciplinary collaboration. Future efforts should focus on: validating mitochondrial function biomarkers such as circulating mtDNA and mitochondria-specific metabolites; refining patient stratification based on mitochondrial dysfunction phenotypes (such as metabolic imbalance type, oxidative stress type); and advancing therapeutic strategies targeting mitochondrial quality control, metabolism, and redox balance. This will translate deep mechanistic insights into effective solutions for improving the clinical management of hepatic fibrosis.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2025.1716765</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2025.1716765</link>
        <title><![CDATA[Role of mitophagy in breast cancer: mitophagy-apoptosis balance and reactive oxygen species play determining role]]></title>
        <pubdate>2026-01-23T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Lung Yiu</author><author>Yan Wah Chong</author><author>Shuyi Yan</author><author>Suk Ying Tsang</author>
        <description><![CDATA[This review aims to present a current overview of the role of mitophagy in breast cancer progression, especially from the point of view of when the cancer is in the untreated state or under chemotherapeutic treatment. We aim to explain the apparently contradictory results as reported in numerous studies on the differential role of mitophagy in breast cancer. We propose that different levels of reactive oxygen species (ROS), and the balance between mitophagy and apoptosis under different conditions are the major reasons to explain for the “discrepancy”. If the cancer cells are untreated, a medium level of ROS promotes cancer progression. Mitophagy inhibition, which leave the dysfunctional mitochondria to generate more ROS, would therefore increase cancer progression. On the other hand, if the cancer cells are undergoing chemotherapeutic treatment, the excessively high level of ROS generated would stimulate both mitophagy and apoptosis, where mitophagy would inhibit apoptosis. In this case, inhibiting mitophagy would potentiate apoptosis and therefore enhance treatment effectiveness. The molecular mechanisms underlying the regulation between mitophagy and apoptosis are also discussed in this review. In summary, the review shall provide important insights for the role of mitophagy in breast cancer. It is proposed that the identification of the molecules involved in balancing mitophagy and apoptosis, and combined therapeutic strategies are the key areas for future exploration.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2025.1695681</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2025.1695681</link>
        <title><![CDATA[Mitochondrial quality control in neurodegenerative diseases: from molecular mechanisms to natural product therapies]]></title>
        <pubdate>2025-10-16T00:00:00Z</pubdate>
        <category>Systematic Review</category>
        <author>Boxun Chen</author><author>Qing Wang</author><author>Yannan Wang</author><author>Qingzhi Liu</author><author>Weiyue Chen</author><author>Hong Mao</author><author>Jiamin Li</author><author>Qi Liu</author><author>Xue Zhou</author>
        <description><![CDATA[BackgroundNeurodegenerative diseases, such as Alzheimer’s disease, Parkinson’s disease, etc., are a group of complex and heterogeneous disorders characterized by progressive synaptic loss and pathological protein alterations. Mitochondria are the main source of energy produced by neurons and support the high energy consumption of the nervous system. Mitochondrial quality control, involving processes like mitophagy and mitochondrial biogenesis, is crucial for mitochondrial homeostasis, and mitochondrial dysfunction is closely related to neurodegenerative diseases pathogenesis, making targeting mitochondrial quality control a potential therapeutic strategy. Natural products offer benefits such as cost-effectiveness, fewer side effects, and other positive qualities, making them suitable choices as supplements or alternatives to traditional drugs for treating neurodegenerative diseases.MethodsA thorough search was conducted on many databases including Web of Science, PubMed, EMBASE, and MEDLINE to investigate the role of mitochondria in neurodegenerative diseases and the therapeutic effects of natural products.ResultsBy searching the relevant studies on neurodegenerative diseases and mitochondria in recent years, we observed a rise in the number of studies examining the functional characteristics and biological events of mitochondrial quality control systems in neurodegenerative diseases pathogenesis and the potential for natural products regulating mitochondrial quality control to improve neurodegenerative diseases.ConclusionThis review summarizes the functional characteristics and biological events of mitochondrial quality control systems in neurodegenerative diseases pathogenesis, and comprehensively analyzes the pharmacological mechanisms by which natural products regulate mitochondrial quality control to improve neurodegenerative diseases, aiming to provide a scientific basis for further research and new clinical drug development.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2025.1651148</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2025.1651148</link>
        <title><![CDATA[Redox regulation of HIV-1: the thioredoxin pathway, oxidative metabolism, and latency control]]></title>
        <pubdate>2025-09-09T00:00:00Z</pubdate>
        <category>Mini Review</category>
        <author>Jesse F. Mangold</author><author>Talia H. Swartz</author>
        <description><![CDATA[Redox homeostasis is a critical determinant of HIV-1 pathogenesis, influencing viral entry, transcription, latency, and persistence in distinct cellular reservoirs. The thioredoxin (Trx) system, a central antioxidant pathway, modulates the redox state of transcription factors and viral proteins while buffering oxidative stress. Paradoxically, while oxidative signals can drive HIV-1 gene expression, the virus also co-opts host antioxidant systems, such as thioredoxin (Trx) and glutathione (GSH), to support its replication and survival. In this review, we examine the multifaceted roles of the Trx pathway in HIV-1 infection, highlighting how redox regulation influences transcriptional activation through NF-κB and AP-1, and modulates the function of viral proteins, such as Tat. We further explore how oxidative metabolism intersects with redox balance to influence latency, particularly through cell-type-specific mechanisms in CD4+ T cells and myeloid cells. Emerging insights into thioredoxin-interacting protein (TXNIP) reveal a critical interface between glucose metabolism, ROS signaling, and latency control. Notably, interventions targeting redox homeostasis—whether antioxidant or pro-oxidant—exert divergent effects depending on the cellular reservoir, underscoring the need for tailored therapeutic strategies. By integrating redox biology and immunometabolism, we outline potential avenues to either stabilize latency or induce viral reactivation in pursuit of an HIV-1 cure.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2025.1690425</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2025.1690425</link>
        <title><![CDATA[Correction: Advances in mitochondrial dysfunction in radiation tissue injury]]></title>
        <pubdate>2025-09-02T00:00:00Z</pubdate>
        <category>Correction</category>
        <author>Jianhuang Rong</author><author>Qiujie Yu</author><author>Guilin Huang</author><author>Yueyue Wang</author><author>Nini Zhang</author>
        <description></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2025.1660330</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2025.1660330</link>
        <title><![CDATA[Advances in mitochondrial dysfunction in radiation tissue injury]]></title>
        <pubdate>2025-08-20T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Jianhuang Rong</author><author>Qiujie Yu</author><author>Guilin Huang</author><author>Yueyue Wang</author><author>Nini Zhang</author>
        <description><![CDATA[Radiation-induced tissue injury is a major limitation in cancer radiotherapy, often leading to collateral damage in healthy tissues. While the nucleus has long been considered the principal target of ionizing radiation, emerging evidence underscores the pivotal role of mitochondria in mediating radiation-induced damage. This review provides a comprehensive overview of mitochondrial dysfunction in various irradiated tissues, including the intestine, hematopoietic system, heart, lung, brain, and skin. Key mitochondrial alterations—such as disrupted dynamics, impaired energy metabolism, excessive reactive oxygen species (ROS) production, and activation of apoptotic and senescence pathways—are highlighted as central mechanisms underlying radiation pathology. Additionally, we summarize the involvement of crucial signaling pathways such as AMP-activated protein kinase/peroxisome proliferator-activated receptor gamma coactivator 1-alpha (AMPK/PGC-1α),nuclear factor erythroid 2–related factor 2/antioxidant response element/mitochondrial transcription factor A (Nrf2/ARE/TFAM), and NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome in regulating mitochondrial responses to radiation stress. A deeper understanding of mitochondrial involvement provides novel avenues for radioprotection and therapeutic interventions in oncology.]]></description>
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