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        <title>Frontiers in Physiology | Developmental Physiology section | New and Recent Articles</title>
        <link>https://www.frontiersin.org/journals/physiology/sections/developmental-physiology</link>
        <description>RSS Feed for Developmental Physiology section in the Frontiers in Physiology journal | New and Recent Articles</description>
        <language>en-us</language>
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        <pubDate>2026-05-07T08:00:11.258+00:00</pubDate>
        <ttl>60</ttl>
        <item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1773684</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1773684</link>
        <title><![CDATA[Perinatal vulnerability: its impact on oral and craniofacial hard tissue development]]></title>
        <pubdate>2026-05-05T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Takehito Ono</author>
        <description><![CDATA[Advances in perinatal and neonatal medicine have dramatically improved the survival rates of infants with perinatal vulnerabilities of preterm birth (PTB), low birth weight (LBW) or small for gestational age (SGA), by rescuing these infants from immediate postnatal complications. Despite improved survival from such problems, it has in turn highlighted long-term complications, including psychiatric, neurological, respiratory, cardiovascular and metabolic diseases. In the oral and craniofacial regions, perinatal vulnerability is associated with an increased risk of developmental complications, including bone deformities, malocclusion and tooth malformations. These anomalies are often tangible and can be recognized earlier than extracranial sequelae; thus, they may serve as accessible indicators for predicting extracranial sequelae that remain latent. Oral and craniofacial sequelae are considered consequences of changes in nutritional status and oxygen saturation before and after birth, which are related to epigenetic changes. Additionally, the development of oral and craniofacial tissues is controlled by mechanical forces. The underlying mechanisms have not been fully elucidated, and future studies elucidating these mechanisms will enhance diagnostic and therapeutic strategies, as well as prognostic accuracy, ultimately improving long-term outcomes for infants born with perinatal vulnerabilities.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1761135</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1761135</link>
        <title><![CDATA[Hyperoxia promotes bronchopulmonary dysplasia via Noggin-mediated BMP4 antagonism and cellular senescence]]></title>
        <pubdate>2026-04-20T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Jiaxin Zhang</author><author>Jia Quan</author><author>Yifan Luo</author><author>Zongli Zhang</author><author>Tao Li</author><author>Shibing Xi</author>
        <description><![CDATA[Bronchopulmonary dysplasia (BPD) represents the most prevalent chronic pulmonary complication in preterm infants, with incompletely understood pathophysiological mechanisms. Hyperoxia exposure constitutes a major risk factor for BPD development, inducing cellular senescence that impairs alveolar maturation. While senescence is predominantly mediated by the p53/p21 signaling pathway, upstream regulatory mechanisms remain inadequately defined. This study aimed to identify critical genes through bioinformatics and elucidate the molecular mechanisms by which the Noggin-BMP4 signaling axis mediates cellular senescence in BPD pathogenesis. Integrating BPD transcriptomic datasets with aging-related databases via WGCNA, Noggin was identified as a hub gene linking BPD and cellular senescence (AUC = 0.80). In HPMECs exposed to 85% hyperoxia, Noggin expression increased approximately 2.5-fold (mRNA) and 2.0-fold (protein), while BMP4 decreased to 50% of controls, accompanied by elevated p53 and p21 expression and positive SA-β-gal staining. Noggin silencing restored BMP4 expression and significantly attenuated hyperoxia-induced p53/p21 upregulation, suggesting that Noggin promotes senescence by suppressing BMP4. In a neonatal rat hyperoxia-induced BPD model, alveolar simplification was observed alongside a threefold increase in Noggin mRNA, a reduction of BMP4 to 30% of controls, and elevated p53/p21 at day 14, corroborating the in vitro findings. These findings suggest that hyperoxia upregulates Noggin to antagonize BMP4 signaling, thereby activating p53/p21-mediated senescence and contributing to alveolar developmental arrest. The Noggin–BMP4 axis may represent a potential therapeutic target for BPD.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1788194</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1788194</link>
        <title><![CDATA[Advances in the study of juvenile hormone signaling]]></title>
        <pubdate>2026-04-15T00:00:00Z</pubdate>
        <category>Systematic Review</category>
        <author>Yue Gao</author>
        <description><![CDATA[Juvenile hormone (JH) and 20-hydroxyecdysone (20E) synergistically regulate the timely onset of metamorphosis during insect metamorphosis. JH regulates multiple physiological processes during insect development via two distinct pathways: intracellular signaling and membrane signaling. Since the discovery of intracellular receptors in Drosophila melanogaster, the mechanism of JH intracellular signaling has been well understood, whereas the study of JH membrane signaling has been relatively slow. In recent years, with the optimization of phosphorylated protein detection technology and improvements in sensitivity, the study of JH membrane receptors and the molecular regulation of membrane signaling has made significant progress. In this paper, we provide an overview of JH intracellular and membrane signaling pathways, with a focus on JH membrane signaling, including induced physiological phenomena, potential membrane receptors, downstream phosphorylation cascades, and interactions between JH membrane signaling and hormone signaling.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1759386</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1759386</link>
        <title><![CDATA[The indirect pathway hypothesis of schizophrenia: insights from perinatal asphyxia]]></title>
        <pubdate>2026-03-16T00:00:00Z</pubdate>
        <category>Mini Review</category>
        <author>Pablo Vázquez-Borsetti</author>
        <description><![CDATA[The comorbidity between perinatal asphyxia (PA) and schizophrenia spectrum disorders (SSD) has been consistently documented in both clinical and experimental research. Individuals exposed to PA show an increased risk of developing long-term neuropsychiatric conditions, including SSD. Experimental models reveal that PA disrupts neurodevelopmental processes also altered in SSD. Moreover, converging evidence indicates that PA can affect the maturation and functional balance of basal ganglia circuits, particularly the indirect pathway, which relies heavily on D2 receptor–mediated signaling and is consistently implicated in the pathophysiology of SSD. Alterations in this pathway may therefore represent a mechanistic link contributing to the shared vulnerability between PA and SSD, where thalamic disinhibition resulting from indirect pathway dysfunction reduces the filtering of information relayed from the thalamus to the cortex, thereby facilitating the emergence of positive symptoms.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1778006</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1778006</link>
        <title><![CDATA[GDM as a unique pathophysiological entity or a transitional pregnancy-induced glucose metabolism abnormality identifying primary diabetes types?]]></title>
        <pubdate>2026-02-27T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Vendula Bartáková</author><author>Eliška Ambrožová</author><author>Petr Žák</author><author>Kateřina Kaňková</author>
        <description><![CDATA[Gestational diabetes mellitus is defined as glucose intolerance first diagnosed during pregnancy; however, this diagnosis may actually represent a heterogeneous spectrum of primary diabetes phenotypes unmasked by the metabolic stress of pregnancy rather than a single pathophysiological entity. The current review aims to summarise available knowledge about the diabetes spectrum in pregnancy with particular focus on its pathophysiology, risk factors and postpartum destiny. Another aim was to discuss possibilities for stratification of the women according to their immediate and future risks of postpartum persistence of glucose intolerance and its complications in later life. Specific objectives of the paper are: (1) to summarise data on physiological metabolic changes in pregnancy, (2) characterise the diabetes spectrum in pregnancy, (3) address the current state of the art in GDM diagnosis and management, (4) to summarize data on postnatal development and maturation of the infants who experienced GDM in utero and, finally (5) discuss possibilities to stratify GDM women according to the later risk for persistence of glucose intolerance after delivery.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2024.1488152</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2024.1488152</link>
        <title><![CDATA[Chronic fetal hypoxia and antenatal Vitamin C exposure differentially regulate molecular signalling in the lung of female lambs in early adulthood]]></title>
        <pubdate>2025-01-15T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Erin V. McGillick</author><author>Sandra Orgeig</author><author>Beth J. Allison</author><author>Kirsty L. Brain</author><author>Melanie R. Bertossa</author><author>Stacey L. Holman</author><author>Ashley S. Meakin</author><author>Michael D. Wiese</author><author>Youguo Niu</author><author>Nozomi Itani</author><author>Katie L. Skeffington</author><author>Christian Beck</author><author>Kimberly J. Botting-Lawford</author><author>Janna L. Morrison</author><author>Dino A. Giussani</author>
        <description><![CDATA[IntroductionChronic fetal hypoxia is commonly associated with fetal growth restriction and can predispose to respiratory disease at birth and in later life. Antenatal antioxidant treatment has been investigated to overcome the effects of oxidative stress in utero to improve respiratory outcomes. We aimed to determine if the effects of chronic fetal hypoxia and antenatal antioxidant administration persist in the lung in early adulthood.MethodsChronically catheterised pregnant sheep were exposed to normoxia (N; n = 20) or hypoxia (H; n = 18; 10% O2) ± maternal daily i. v. saline (N = 11; H = 8) or Vitamin C (VC; NVC = 9; HVC = 10) from 105 to 138 days (term, ∼145 days). Lungs were collected from female lambs 9 months after birth (early adulthood). Lung tissue expression of genes and proteins regulating oxidative stress, mitochondrial function, hypoxia signalling, glucocorticoid signalling, surfactant maturation, inflammation and airway remodelling were measured.ResultsChronic fetal hypoxia upregulated lung expression of markers of prooxidant, surfactant lipid transport and airway remodelling pathways in early adulthood. Antenatal Vitamin C normalized prooxidant and airway remodelling markers, increased endogenous antioxidant, vasodilator and inflammatory markers, and altered regulation of hypoxia signalling and glucocorticoid availability.ConclusionThere are differential effects of antenatal Vitamin C on molecular markers in the lungs of female lambs from normoxic and hypoxic pregnancy in early adulthood.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2024.1490154</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2024.1490154</link>
        <title><![CDATA[Effects of hypoxia on uteroplacental and fetoplacental vascular function during pregnancy]]></title>
        <pubdate>2024-12-18T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Germán A. Arenas</author><author>Ramón A. Lorca</author>
        <description><![CDATA[During pregnancy, marked changes in vasculature occur. The placenta is developed, and uteroplacental and fetoplacental circulations are established. These processes may be negatively affected by genetic anomalies, maternal environment (i.e., obesity or diabetes), and environmental conditions such as pollutants and hypoxia. Chronic hypoxia has detrimental effects on the vascular adaptations to pregnancy and fetal growth. The typical pregnancy-dependent rise in uterine blood flow by vascular remodeling and vasodilation of maternal uterine arteries is reduced, leading to increases in vascular tone. These maladaptations may lead to complications such as fetal growth restriction (FGR) and preeclampsia. In this review, the effect of hypoxia on uteroplacental and fetoplacental circulation and its impact on pregnancy outcomes in humans and animal models are discussed. Evidence is provided for several mechanisms that affect pregnancy through hypoxia-induced alterations. Future directions to fill gaps in knowledge and develop therapeutic strategies to prevent or alleviate hypoxia-related pregnancy complications, such as FGR and preeclampsia, are suggested.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2024.1442000</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2024.1442000</link>
        <title><![CDATA[Nonlinear pathological trajectory of a high-myopia C57/BL6J mouse model induced by form deprivation]]></title>
        <pubdate>2024-10-30T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Yue Wen</author><author>Yan Li</author><author>Li Zhu</author><author>Tao Tang</author><author>Huichao Yan</author><author>Jie Hu</author><author>Kai Wang</author><author>Mingwei Zhao</author><author>Qiong Xu</author>
        <description><![CDATA[IntroductionTo establish a high myopia model in C57BL/6J mice with monocular form deprivation myopia (FDM) and investigate its ocular structure pathological trajectory.MethodsHealthy 3-week-old C57BL/6J mice were divided into an FDM group (n = 36) and a control group (n = 24). The left eyes of the FDM group were patched, while the right eyes served as controls. Biometric parameters and fundus morphology were assessed at baseline and after 4, 8, and 12 weeks of form deprivation.ResultsSignificant differences were observed in the deprived eyes, including longer axial length, higher refractive power, deeper vitreous chambers, thinner retina, choroid, and sclera, and smaller scleral fibers’ diameters under a transmission electron microscope. Retinal vascular area proportion in covered eyes decreased significantly (P < 0.05), with a decline rate of 11% from weeks 4 to 8 and a faster decline of 19% from weeks 8 to 12, while this proportion increased significantly in control eyes.DiscussionThis study successfully induced a high myopia model in mice with long-term form deprivation. The axial length grew dramatically in FDM in the first 8 weeks, while the pathological progress of the fundus accelerated from weeks 8 to 12.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2024.1415746</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2024.1415746</link>
        <title><![CDATA[Role of nuclear protein Akirin in the modulation of female reproduction in Nilaparvata lugens (Hemiptera: Delphacidae)]]></title>
        <pubdate>2024-07-09T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Feiyan Gou</author><author>Daowei Zhang</author><author>Siqi Chen</author><author>Mingjing Zhang</author><author>Jing Chen</author>
        <description><![CDATA[Introduction: Akirin as a highly conserved transcription factor, exerts a profound influence on the growth, development, immune response, and reproductive processes in animals. The brown planthopper (BPH), Nilaparvata lugens, a major pest in rice production in Asia, possesses high reproductive capacity, a critical factor contributing to reduced rice yields. The aims of this study were to demonstrate the regulatory role of Akirin in the reproduction of BPH.Methods: In this study, quantitative PCR (qPCR) was used to detect the mRNA expression of genes. RNA interference (RNAi) was used to downregulate the expression of Akirin gene, and RNA sequencing (RNA-seq) was used to screen for differentially expressed genes caused by Akirin downregulation. Hormone contents were measured with the enzyme linked immunosorbent assay (ELISA), and protein content was evaluated with the bicinchoninic acid (BCA) method.Results: Using BPH genome data, we screened for an Akirin gene (NlAkirin). An analysis of tissue-specific expressions showed that NlAkirin was expressed in all tissues tested in female BPH, but its expression level was highest in the ovary. After inhibiting the mRNA expression of NlAkirin in BPH females, the number of eggs laid, hatching rate, and number of ovarioles decreased. Transcriptome sequencing was performed, following a NlAkirin double-stranded RNA treatment. Compared with the genes of the control, which was injected with GFP double-stranded RNA, there were 438 upregulated genes and 1012 downregulated genes; the expression of vitellogenin (Vg) and vitellogenin receptor (VgR) genes as well as the mRNA expression of genes related to the target of rapamycin (TOR), juvenile hormone (JH), and insulin pathways involved in Vg synthesis was significantly downregulated. As a result of NlAkirin knockdown, the titers of JH III and Ecdysone (Ecd) were downregulated in unmated females but returned to normal levels in mated females. The ovarian protein contents in both unmated and mated females were downregulated.Discussion and conclusion: Our results suggest that NlAkirin affects female BPH reproduction by regulating the mRNA expression of genes related to the Vg, VgR, TOR, JH, and insulin signaling pathways, in addition to the titers of JH III and Ecd. The findings of this research provide novel insights into the regulatory role of Akirin in insect reproductive capacity.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2024.1340441</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2024.1340441</link>
        <title><![CDATA[Analysis of fetal heart rate fluctuations in women diagnosed with preeclampsia during the latent phase of labor]]></title>
        <pubdate>2024-05-23T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Nancy B. Lucero-Orozco</author><author>José Javier Reyes-Lagos</author><author>María del Rocío Ortíz-Pedroza</author><author>Ana Karen Talavera-Peña</author><author>Eric Alonso Abarca-Castro</author><author>Hugo Mendieta-Zerón</author><author>Adriana Cristina Pliego-Carrillo</author><author>Jorge Rodríguez-Arce</author><author>Luis Adrián Zúñiga-Avilés</author><author>Laura Mercedes Santiago-Fuentes</author><author>Claudia Ivette Ledesma-Ramírez</author><author>Miguel Ángel Peña-Castillo</author>
        <description><![CDATA[IntroductionFetal heart rate variability (fHRV) is a tool used to investigate the functioning of the fetal autonomic nervous system. Despite the significance of preeclampsia, fHRV during the latent phase of labor has not been extensively studied. This study aimed to evaluate fetal cardiac autonomic activity by using linear and nonlinear indices of fHRV analysis in women diagnosed with preeclampsia without hypertensive treatment during gestation, compared to normotensive women during the latent phase of labor.MethodsA cross-sectional and exploratory study was conducted among pregnant women in the latent phase of labor, forming three study groups: normotensive or control (C, 38.8 ± 1.3 weeks of pregnancy, n = 22), preeclampsia with moderate features (P, 37.6 ± 1.4 weeks of pregnancy n = 10), and preeclampsia with severe features (SP, 36.9 ± 1.2 weeks of pregnancy, n = 12). None of the participants received anti-hypertensive treatment during their pregnancy. Linear and nonlinear features of beat-to-beat fHRV, including temporal, frequency, symbolic dynamics, and entropy measures, were analyzed to compare normotensive and preeclamptic groups.ResultsSignificantly lower values of multiscale entropy (MSE) and short-term complexity index (Ci) were observed in the preeclamptic groups compared to the C group (p < 0.05). Additionally, higher values of SDNN (standard deviation of R-R intervals) and higher values of low-frequency power (LF) were found in the P group compared to the C group.ConclusionOur findings indicate that changes in the complexity of fetal heart rate fluctuations may indicate possible disruptions in the autonomic nervous system of fetuses in groups affected by undiagnosed preeclampsia during pregnancy. Reduced complexity and shifts in fetal autonomic cardiac activity could be associated with preeclampsia’s pathophysiological mechanisms during the latent phase of labor.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2024.1394707</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2024.1394707</link>
        <title><![CDATA[Impact of maternal posture on fetal physiology in human pregnancy: a narrative review]]></title>
        <pubdate>2024-05-17T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Allan J. Kember</author><author>Jennifer L. Anderson</author><author>Sarah C. House</author><author>David G. Reuter</author><author>Craig J. Goergen</author><author>Sebastian R. Hobson</author>
        <description><![CDATA[In numerous medical conditions, including pregnancy, gravity and posture interact to impact physiology and pathophysiology. Recent investigations, for example, pertaining to maternal sleeping posture during the third trimester and possible impact on fetal growth and stillbirth risk highlight the importance and potential clinical implications of the subject. In this review, we provide an extensive discussion of the impact of maternal posture on fetal physiology from conception to the postpartum period in human pregnancy. We conducted a systematic literature search of the MEDLINE database and identified 242 studies from 1991 through 2021, inclusive, that met our inclusion criteria. Herein, we provide a synthesis of the resulting literature. In the first section of the review, we group the results by the impact of maternal posture at rest on the cervix, uterus, placenta, umbilical cord, amniotic fluid, and fetus. In the second section of the review, we address the impact on fetal-related outcomes of maternal posture during various maternal activities (e.g., sleep, work, exercise), medical procedures (e.g., fertility, imaging, surgery), and labor and birth. We present the published literature, highlight gaps and discrepancies, and suggest future research opportunities and clinical practice changes. In sum, we anticipate that this review will shed light on the impact of maternal posture on fetal physiology in a manner that lends utility to researchers and clinicians who are working to improve maternal, fetal, and child health.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2024.1424967</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2024.1424967</link>
        <title><![CDATA[Editorial: Regulatory network in embryonic development and implantation]]></title>
        <pubdate>2024-05-14T00:00:00Z</pubdate>
        <category>Editorial</category>
        <author>Yao Xu</author><author>Lin Zhao</author><author>Wenjing Wang</author>
        <description></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2024.1408809</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2024.1408809</link>
        <title><![CDATA[Editorial: Climate change and developmental physiology]]></title>
        <pubdate>2024-04-25T00:00:00Z</pubdate>
        <category>Editorial</category>
        <author>Sukanta Mondal</author><author>Rafael Martinez-Garcia</author>
        <description></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2024.1394120</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2024.1394120</link>
        <title><![CDATA[Editorial: Adverse outcomes of preeclampsia: from mother to baby, pregnancy to postpartum]]></title>
        <pubdate>2024-04-08T00:00:00Z</pubdate>
        <category>Editorial</category>
        <author>Bhavisha A. Bakrania</author><author>Frank T. Spradley</author><author>Lana McClements</author>
        <description></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2024.1348993</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2024.1348993</link>
        <title><![CDATA[A prenatal acoustic signal of heat reduces a biomarker of chronic stress at adulthood across seasons]]></title>
        <pubdate>2024-03-29T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Eve Udino</author><author>Marja A. Oscos-Snowball</author><author>Katherine L. Buchanan</author><author>Mylene M. Mariette</author>
        <description><![CDATA[During development, phenotype can be adaptively modulated by environmental conditions, sometimes in the long-term. However, with weather variability increasing under climate change, the potential for maladaptive long-term responses to environmental variations may increase. In the arid-adapted zebra finch, parents emit “heat-calls” when experiencing heat during incubation, which adaptively affects offspring growth in the heat, and adult heat tolerance. This suggests that heat-call exposure may adjust individual phenotype to hot conditions, potentially compromising individual sensitivity to cool weather conditions. To test this hypothesis, we manipulated individual prenatal acoustic and postnatal thermal experiences during development, and sought to assess subsequent chronic responses to thermal fluctuations at adulthood. We thus measured heterophil to lymphocyte (H/L) ratios in adults, when held in outdoor aviaries during two summers and two winters. We found that birds exposed to heat-calls as embryos, had consistently lower H/L ratios than controls at adulthood, indicative of lower chronic stress, irrespective of the season. Nonetheless, in all birds, the H/L ratio did vary with short-term weather fluctuations (2, 5 or 7 days), increasing at more extreme (low and high) air temperatures. In addition, the H/L ratio was higher in males than females. Overall, while H/L ratio may reflect how individuals were being impacted by temperature, heat-call exposed individuals did not show a stronger chronic response in winter, and instead appeared more resilient to thermal variability than control individuals. Our findings therefore suggest that heat-call exposure did not compromise individual sensitivity to low temperatures at adulthood. Our study also reveals that prenatal sound can lead to long-term differences in individual physiology or quality/condition, as reflected by H/L ratios, which are consistent with previously-demonstrated reproductive fitness differences.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2024.1354327</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2024.1354327</link>
        <title><![CDATA[The interplay of maternal and offspring obesogenic diets: the impact on offspring metabolism and muscle mitochondria in an outbred mouse model]]></title>
        <pubdate>2024-03-22T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Inne Xhonneux</author><author>Waleed F. A. Marei</author><author>Ben Meulders</author><author>Silke Andries</author><author>Jo L. M. R. Leroy</author>
        <description><![CDATA[Consumption of obesogenic (OB) diets increases the prevalence of maternal obesity worldwide, causing major psychological and social burdens in women. Obesity not only impacts the mother’s health and fertility but also elevates the risk of obesity and metabolic disorders in the offspring. Family lifestyle is mostly persistent through generations, possibly contributing to the growing prevalence of obesity. We hypothesized that offspring metabolic health is dependent on both maternal and offspring diet and their interaction. We also hypothesized that the sensitivity of the offspring to the diet may be influenced by the match or mismatch between offspring and maternal diets. To test these hypotheses, outbred Swiss mice were fed a control (C, 10% fat, 7% sugar, and n = 14) or OB diet (60% fat, 20% sugar, and n = 15) for 7 weeks and then mated with the same control males. Mice were maintained on the same corresponding diet during pregnancy and lactation, and the offspring were kept with their mothers until weaning. The study focused only on female offspring, which were equally distributed at weaning and fed C or OB diets for 7 weeks, resulting in four treatment groups: C-born offspring fed C or OB diets (C » C and C » OB) and OB-born offspring fed C or OB diets (OB » C and OB » OB). Adult offspring’s systemic blood profile (lipid and glucose metabolism) and muscle mitochondrial features were assessed. We confirmed that the offspring’s OB diet majorly impacted the offspring’s health by impairing the offspring’s serum glucose and lipid profiles, which are associated with abnormal muscle mitochondrial ultrastructure. Contrarily, maternal OB diet was associated with increased expression of mitochondrial complex markers and mitochondrial morphology in offspring muscle, but no additive effects of (increased sensitivity to) an offspring OB diet were observed in pups born to obese mothers. In contrast, their metabolic profile appeared to be healthier compared to those born to lean mothers and fed an OB diet. These results are in line with the thrifty phenotype hypothesis, suggesting that OB-born offspring are better adapted to an environment with high energy availability later in life. Thus, using a murine outbred model, we could not confirm that maternal obesogenic diets contribute to female familial obesity in the following generations.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2024.1332946</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2024.1332946</link>
        <title><![CDATA[Mechanisms of endometrial aging: lessons from natural conceptions and assisted reproductive technology cycles]]></title>
        <pubdate>2024-02-28T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Anat Chemerinski</author><author>Jessica Garcia de Paredes</author><author>Kristin Blackledge</author><author>Nataki C. Douglas</author><author>Sara S. Morelli</author>
        <description><![CDATA[Until recently, the study of age-related decline in fertility has focused primarily on the ovary; depletion of the finite pool of oocytes and increases in meiotic errors leading to oocyte aneuploidy are well-established mechanisms by which fertility declines with advancing age. Comparatively little is known about the impact of age on endometrial function. The endometrium is a complex tissue comprised of many cell types, including epithelial, stromal, vascular, immune and stem cells. The capacity of this tissue for rapid, cyclic regeneration is unique to this tissue, undergoing repeated cycles of growth and shedding (in the absence of an embryo) in response to ovarian hormones. Furthermore, the endometrium has been shown to be capable of supporting pregnancies beyond the established boundaries of the reproductive lifespan. Despite its longevity, molecular studies have established age-related changes in individual cell populations within the endometrium. Human clinical studies have attempted to isolate the effect of aging on the endometrium by analyzing pregnancies conceived with euploid, high quality embryos. In this review, we explore the existing literature on endometrial aging and its impact on pregnancy outcomes. We begin with an overview of the principles of endometrial physiology and function. We then explore the mechanisms behind endometrial aging in its individual cellular compartments. Finally, we highlight lessons about endometrial aging gleaned from rodent and human clinical studies and propose opportunities for future study to better understand the contribution of the endometrium to age-related decline in fertility.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2024.1331098</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2024.1331098</link>
        <title><![CDATA[Understanding bovine embryo elongation: a transcriptomic study of trophoblastic vesicles]]></title>
        <pubdate>2024-01-29T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Séverine A. Degrelle</author><author>Fulin Liu</author><author>Denis Laloe</author><author>Christophe Richard</author><author>Daniel Le Bourhis</author><author>Marie-Noëlle Rossignol</author><author>Isabelle Hue</author>
        <description><![CDATA[Background: During the process of elongation, the embryo increases in size within the uterus, while the extra-embryonic tissues (EETs) develop and differentiate in preparation for implantation. As it grows, the ovoid embryo transforms into a tubular form first and then a filamentous form. This process is directed by numerous genes and pathways, the expression of which may be altered in the case of developmental irregularities such as when the conceptus is shorter than expected or when the embryo develops after splitting. In bovines, efforts to understand the molecular basis of elongation have employed trophoblastic vesicles (TVs)—short tubular EET pieces that lack an embryo—which also elongate in vivo. To date, however, we lack molecular analyses of TVs at the ovoid or filamentous stages that might shed light on the expression changes involved.Methods: Following in vivo development, we collected bovine conceptuses from the ovoid (D12) to filamentous stages (D18), sectioned them into small pieces with or without their embryonic disc (ED), and then, transferred them to a receptive bovine uterus to assess their elongation abilities. We also grew spherical blastocysts in vitro up to D8 and subjected them to the same treatment. Then, we assessed the differences in gene expression between different samples and fully elongating controls at different stages of elongation using a bovine array (10 K) and an extended qPCR array comprising 224 genes across 24 pathways.Results:In vivo, TVs elongated more or less depending on the stage at which they had been created and the time spent in utero. Their daily elongation rates differed from control EET, with the rates of TVs sometimes resembling those of earlier-stage EET. Overall, the molecular signatures of TVs followed a similar developmental trajectory as intact EET from D12–D18. However, within each stage, TVs and intact EET displayed distinct expression dynamics, some of which were shared with other short epithelial models.Conclusion: Differences between TVs and EET likely result from multiple factors, including a reduction in the length and signaling capabilities of TVs, delayed elongation from inadequate uterine signals, and modified crosstalk between the conceptus and the uterus. These findings confirm that close coordination between uterine, embryonic, and extra-embryonic tissues is required to orchestrate proper elongation and, based on the partial differentiation observed, raise questions about the presence/absence of certain developmental cues or even their asynchronies.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2023.1351594</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2023.1351594</link>
        <title><![CDATA[Editorial: Environmental toxicity in reproduction]]></title>
        <pubdate>2023-12-19T00:00:00Z</pubdate>
        <category>Editorial</category>
        <author>Jiahui Ding</author><author>Yong Song</author><author>Chunyan Liu</author><author>Marianna Sadagurski</author>
        <description></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2023.1346913</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2023.1346913</link>
        <title><![CDATA[Editorial: Placental physiology and placental derived stem cells for regenerative medicine]]></title>
        <pubdate>2023-12-14T00:00:00Z</pubdate>
        <category>Editorial</category>
        <author>Jitendra K. Kanaujiya</author><author>Jay S. Mishra</author>
        <description></description>
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