American journal of physiology. Cell physiology最新文献

{"title":"Obesity and type 2 diabetes mellitus: insights from skeletal muscle extracellular matrix remodeling.","authors":"Linda Wu, Dawn K Coletta","doi":"10.1152/ajpcell.00154.2024","DOIUrl":"https://doi.org/10.1152/ajpcell.00154.2024","url":null,"abstract":"<p><p>Obesity and type 2 diabetes mellitus (T2DM) are metabolic diseases at epidemic proportions. The economic burden for these diseases is at an all-time high, and as such, there is an urgent need for advancements in identifying targets for treating these complex disorders. The extracellular matrix (ECM), comprising collagen, fibronectin, laminin, elastin, and proteoglycan, surrounds skeletal muscles and plays a critical role in maintaining tissue homeostasis by providing structural support and facilitating cell-to-cell communication. Disruption of the ECM signaling results in changes to its micro/macroenvironment, thereby modifying tissue homeostasis. Skeletal muscle ECM remodeling has been shown to be associated with insulin resistance, an underlying feature of obesity and T2DM. This narrative review explores the critical components of skeletal muscle ECM and its accumulation and remodeling in metabolic diseases. In addition, we discuss potential treatments to mitigate the effects of ECM remodeling in skeletal muscle. We conclude that targeting ECM remodeling in skeletal muscle represents a promising yet underexplored therapeutic avenue in the management of metabolic disorders.</p>","PeriodicalId":7585,"journal":{"name":"American journal of physiology. Cell physiology","volume":"328 6","pages":"C1752-C1763"},"PeriodicalIF":5.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143955952","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Inflammation in cancer cachexia: still the central tenet or just another player?","authors":"Noemi Iaia, Chiara Noviello, Maurizio Muscaritoli, Paola Costelli","doi":"10.1152/ajpcell.00808.2024","DOIUrl":"10.1152/ajpcell.00808.2024","url":null,"abstract":"<p><p>Cancer cachexia, a multifactorial syndrome characterized by body weight loss, muscle, and adipose tissue wasting, affects patients with cancer. Over time, the definition of cachexia has been modified, including inflammation as one of the main causal factors. Evidence has suggested that a range of proinflammatory mediators may be involved in the regulation of intracellular signaling, resulting in enhanced resting energy expenditure, metabolic changes, and muscle atrophy, all of which are typical features of cachexia. Physiologically speaking, however, inflammation is a response aimed at facing potentially damaging events. Along this line, its induction in the cancer hosts could be an attempt to restore the physiological homeostasis. Interesting observations have shown that cytokines such as interleukins 4 and 6 could improve muscle wasting, supporting the view that the same mediator may exert pro- or anti-inflammatory activity depending on the immune cells involved as well as on the tissue metabolic demand. In conclusion, whether inflammation is crucial to the occurrence of cachexia or just one contributor among others, is still unclear. Indeed, while inflammation is a trigger of cachexia, the alterations of energy and protein metabolism and of the hormonal homeostasis occurring in cachexia likely act as inflammatory stimuli on their own. Whether the causative role prevails over the compensatory one likely depends on the tumor type and stage, patient lifestyle, the presence of comorbidities, and the response to anticancer treatments paving the way to a holistic, personalized approach to cancer cachexia.</p>","PeriodicalId":7585,"journal":{"name":"American journal of physiology. Cell physiology","volume":" ","pages":"C1837-C1852"},"PeriodicalIF":5.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143968176","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Unraveling the functional and molecular interplay between cellular senescence and the unfolded protein response.","authors":"Joëlle Giroud, Emilie Combémorel, Albin Pourtier, Corinne Abbadie, Olivier Pluquet","doi":"10.1152/ajpcell.00091.2025","DOIUrl":"https://doi.org/10.1152/ajpcell.00091.2025","url":null,"abstract":"<p><p>Senescence is a complex cellular state that can be considered as a stress response phenotype. A decade ago, we suggested the intricate connections between unfolded protein response (UPR) signaling and the development of the senescent phenotype. Over the past ten years, significant advances have been made in understanding the multifaceted role of the UPR in regulating cellular senescence, highlighting its contribution to biological processes such as oxidative stress and autophagy. In this updated review, we expand these interconnections with the benefit of new insights, and we suggest that targeting specific components of the UPR could provide novel therapeutic strategies to mitigate the deleterious effects of senescence, with significant implications for age-related pathologies and geroscience.</p>","PeriodicalId":7585,"journal":{"name":"American journal of physiology. Cell physiology","volume":"328 6","pages":"C1764-C1782"},"PeriodicalIF":5.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143961003","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mechanometabolism: recent findings on the intersection of cell adhesion, cell migration, and metabolism.","authors":"Emily D Fabiano, Jenna M Poole, Cynthia A Reinhart-King","doi":"10.1152/ajpcell.00892.2024","DOIUrl":"10.1152/ajpcell.00892.2024","url":null,"abstract":"<p><p>Chemical and mechanical cues within the extracellular matrix (ECM) can initiate intracellular signaling that changes an array of fundamental cell functions. In recent work, studies of cell-ECM adhesion have deepened to include the influence of the physical ECM on cell metabolism. Since many biological processes involve metabolic programs, changes to cellular metabolism in response to cues in the ECM can have marked effects on cell health. In this review, we describe molecular mechanisms associated with cell-ECM adhesion that are key players in metabolism-induced changes to cell behaviors, including migration. We first review how changes to metabolite availability in the extracellular environment or manipulation of metabolic machinery in cells impact focal adhesions. We then connect this work to recent findings regarding the reverse relationship, namely, how the manipulation of focal adhesion proteins or integrins feeds back to alter cell metabolism. Finally, we consider the latest findings from studies that describe how the mechanical properties of the ECM, primarily stiffness and confinement, alter cellular metabolism. We identify key areas of future investigation that may elucidate the molecular drivers that permit cells to respond to mechanical and chemical ECM cues by reprogramming their metabolism to better inform future diagnostics and therapeutics for disease states.</p>","PeriodicalId":7585,"journal":{"name":"American journal of physiology. Cell physiology","volume":" ","pages":"C1866-C1879"},"PeriodicalIF":5.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143952249","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sixteen weeks of high-speed treadmill running is insufficient to induce Achilles tendinopathy in a rat model.","authors":"Snehal S Shetye, Margaret K Tamburro, Ashley K Fung, Thomas P Leahy, Madison N Magee, Harina A Raja, Stephanie N Weiss, Courtney A Nuss, Daniel C Farber, Louis J Soslowsky","doi":"10.1152/ajpcell.00186.2025","DOIUrl":"10.1152/ajpcell.00186.2025","url":null,"abstract":"<p><p>Despite the high prevalence of Achilles tendinopathy, clinically relevant animal models of Achilles tendinopathy are lacking. Previous studies have demonstrated possible tendinopathic cell and matrix changes with high-speed treadmill running, but the consistency as well as functional and mechanical consequences of these changes were unclear. We sought to determine the applicability of this protocol as a tendinopathy model by defining changes in Achilles tendon structure, function, and mechanics associated with 16 wk of high-speed treadmill running (26.8 m/min, 60 min/day, and 5 days/wk). We expected that high-speed running would induce detrimental structural, functional, and mechanical changes that worsen over the course of the 16-wk protocol. Treadmill running did influence body weight, hindlimb gait, and tendon cross-sectional area. However, contrary to our hypothesis, treadmill running did not induce tendinopathic changes in matrix organization, cell morphology, or tendon mechanics. As such, alternative strategies for robust and reproducible induction of Achilles tendinopathy in preclinical animal models are needed.<b>NEW & NOTEWORTHY</b> We demonstrated that 16 wk of high-speed treadmill running did not induce structural, functional, or mechanical changes consistent with Achilles tendinopathy in the rat. These findings underscore the importance of exploring alternative approaches to generating reliable and clinically relevant animal models of Achilles tendinopathy.</p>","PeriodicalId":7585,"journal":{"name":"American journal of physiology. Cell physiology","volume":" ","pages":"C2013-C2022"},"PeriodicalIF":5.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12151315/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143966275","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Comprehensive evaluation and application of tissue clearing techniques for 3-D visualization of splenic neural and immune architecture.","authors":"Jianing Li, Letian He, Wenling Wang, Siyu Wang, Dan Zhang, Liyun Liang, Guangping Song, Yijian Zhang, Shaoqing Yu, Lei Wang, Qiuying Han, Shaoyi Huang, Sen Li, Haiqing Tu, Zengqing Song, Huaibin Hu, Huiyan Li, Yang Yang, Min Wu","doi":"10.1152/ajpcell.00084.2025","DOIUrl":"https://doi.org/10.1152/ajpcell.00084.2025","url":null,"abstract":"<p><p>As the largest secondary lymphoid organ, the spleen plays a crucial role in initiating and sustaining immune responses against blood-borne pathogens through antigen capture and delivery. It is innervated by both autonomic and sensory nerves, which allows for neural modulation of its immune responses. The intricate spatial structure and precise coordination between immune and neural components are essential for proper splenic function, necessitating three-dimensional (3-D) imaging to reveal its architecture. However, the dense fibrous capsule and exceptionally rich vasculature of the spleen pose significant challenges for achieving comprehensive 3-D visualization of the entire organ. Here, we systematically evaluated and compared five cutting-edge tissue clearing approaches-ImmuView, fast light-microscopic analysis of antibody-stained whole organs, small-micelle-mediated human organ efficient clearing and labeling (SHANEL), advanced clear, unobstructed brain imaging cocktails and computational analysis (advanced CUBIC), and clearing-enhanced 3-D microscopy-for their effectiveness in rendering the spleen transparent for multiplexed antibody staining and high-resolution 3-D imaging. Our results indicated that SHANEL provided the clearest visualization of essential splenic neural and immune components. Meanwhile, advanced CUBIC achieved the greatest labeling efficacy for immune cells, albeit with slightly reduced transparency. Importantly, our study marked the first application of these optimized protocols to human spleen tissue, successfully revealing the highly organized immune cell zones and neural networks with enhanced clarity. Notably, we identified the nociceptive sensory innervation within human spleen tissue for the first time. Collectively, these findings establish optimal imaging strategies for visualizing splenic immune cells and neural structure in both murine and human tissues, providing profound insights into the intricate neuroimmune interactions and their pivotal roles in the immune functions of the spleen.<b>NEW & NOTEWORTHY</b> This study systematically assessed five tissue-clearing techniques and optimized the conditions of each protocol to overcome the challenges of splenic 3-D imaging posed by its dense structure and high pigmentation. The results demonstrated SHANEL and advanced CUBIC as the optimal methods for 3-D visualization of diverse splenic immune and neural architecture, with which we successfully mapped splenic neuroimmune landscape and identified nociceptive nerves within the human spleen for the first time.</p>","PeriodicalId":7585,"journal":{"name":"American journal of physiology. Cell physiology","volume":"328 6","pages":"C1699-C1715"},"PeriodicalIF":5.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143960887","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Extracellular matrix matters: matrix-based bioscaffolds in advancing translational cancer research and targeted therapy.","authors":"Nikos K Karamanos, Zoi Piperigkou, Chrisavgi Gourdoupi, Sylvia Mangani, Maria dM Vivanco","doi":"10.1152/ajpcell.00050.2025","DOIUrl":"10.1152/ajpcell.00050.2025","url":null,"abstract":"<p><p>The onset, development, and progression of cancer are greatly influenced by the microenvironmental cues originating from diverse elements within the tumor niche. Extracellular matrix (ECM), the complex and dynamic macromolecular three-dimensional network (3-D), governs cell functionality and plays key roles in tumor growth and spreading. This article highlights the significance of ECM-based bioscaffolds in providing a relevant microenvironment not only for studying tumor behavior and drug efficacy but also for narrowing the gap between translational cancer research and targeted cancer treatment. The development of novel and user-friendly platforms that resemble the human tumor microenvironment in early and advanced cancer stages, may help to predict treatment response, thus facilitating the development and testing of new drugs, bridging the gap between in vitro and in vivo models. In addition, we present innovative strategies leveraging ECM bioscaffolds for personalized cancer treatment, including drug delivery systems and tissue engineering approaches. Specific case studies as well as ethical concerns related to the use of ECM bioscaffolds in research and therapy are also presented and critically discussed. By elucidating the intricate interplay between ECM and cancer biology, this article underscores the potential of ECM bioscaffolds as novel platforms for shaping future therapeutic interventions and advancing precision oncology.</p>","PeriodicalId":7585,"journal":{"name":"American journal of physiology. Cell physiology","volume":" ","pages":"C1957-C1963"},"PeriodicalIF":5.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143539881","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Enteroendocrine cells regulate intestinal barrier permeability.","authors":"Jennifer G Nwako, Sparsh D Patel, Taevon J Roach, Saanvi R Gupte, Samara G Williams, Anne Marie Riedman, Heather A McCauley","doi":"10.1152/ajpcell.01077.2024","DOIUrl":"10.1152/ajpcell.01077.2024","url":null,"abstract":"<p><p>The intestinal epithelial barrier is essential for nutrient absorption and protection against ingested pathogens and foreign substances. Barrier integrity is maintained by tight junctions, which are sensitive to inflammatory signals, thus creating a feed-forward loop with an increasingly permeable barrier that further drives inflammation and is the hallmark of inflammatory bowel disease. There are currently no therapeutic strategies to improve the intestinal epithelial barrier. We hypothesized that enteroendocrine cells may play an unappreciated role in maintaining barrier integrity. To test this hypothesis, we seeded human intestinal enteroids with genetic loss of enteroendocrine cells on Transwell filters and evaluated transepithelial electrical resistance, paracellular permeability, and the localization and abundance of junctional proteins. We found that enteroendocrine cells were required to maintain a healthy barrier in crypt-like \"stem\" and villus-like differentiated cultures. In addition, exogenous supplementation of enteroendocrine-deficient cultures with the hormones peptide tyrosine-tyrosine (PYY), and the somatostatin analog octreotide was sufficient to rescue many aspects of this barrier defect both at baseline and in the presence of the inflammatory cytokine tumor necrosis factor. Surprisingly, these improvements in barrier function occurred largely independently of changes in protein abundance of junctional proteins zona occludens 1, occludin, and claudin-2. These findings support a novel role for enteroendocrine cells in augmenting epithelial barrier function in the presence of inflammatory stimuli and present an opportunity for developing therapies to improve the intestinal barrier.<b>NEW & NOTEWORTHY</b> There are no therapies that directly improve the permeability of the intestinal epithelial barrier. This work uses a human intestinal epithelial model system to demonstrate that sensory enteroendocrine cells are necessary for healthy barrier function and that two of their secreted products, peptide YY and somatostatin, are sufficient to improve barrier function at homeostasis and in the presence of inflammatory cytokines. This could provide novel treatments for strengthening the epithelial barrier in human gastrointestinal disease.</p>","PeriodicalId":7585,"journal":{"name":"American journal of physiology. Cell physiology","volume":" ","pages":"C1501-C1508"},"PeriodicalIF":5.0,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12054964/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143646946","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The long road to Ithaca: a physiologist's journey.","authors":"Sadis Matalon","doi":"10.1152/ajpcell.00030.2025","DOIUrl":"10.1152/ajpcell.00030.2025","url":null,"abstract":"<p><p>It was an honor to be asked to deliver the Walter B. Cannon Lecture during the 2024 American Physiological Summit meeting. Dr. Cannon served as president of the American Physiological Society from 1914-1916. He coined the term \"fight or flight\" to describe an animal's response to threats and the concept of Homeostasis. He was the consummate physician-scientist, an outstanding mentor and teacher, a prolific writer, and a humanitarian. The title of my lecture is based on a poem entitled \"Ithaca,\" written by the Greek poet C. P. Cavafy, who recounts the 10 yr travels of Ulysses, from Troy to his home, Ithaca. Odysseus had to overcome many obstacles to survive this long journey. Like Odysseus, I encountered myriad of professional and health problems. But, I also have experienced the thrill of contributing to scientific knowledge, the satisfaction of watching my mentees develop into independent scientists, the excitement of teaching respiration physiology to medical and professional students, and the pleasure of being of service to my discipline by serving as Editor of the American Journal of Physiology-Lung Cellular and Molecular Physiology and of Physiological Reviews. During my career, I have been interested in identifying the basic mechanisms by which oxidant gases and pathogens damage the blood gas barrier resulting in acute and chronic lung injury. In this brief review, I summarize the results of current studies implicating free heme as a major mediator of acute lung injury and our efforts to develop recombinant forms of human hemopexin, as a countermeasure.</p>","PeriodicalId":7585,"journal":{"name":"American journal of physiology. Cell physiology","volume":" ","pages":"C1526-C1534"},"PeriodicalIF":5.0,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12216966/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143490526","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A novel lncRNA ABCE1-5 regulates pulmonary fibrosis by targeting KRT14.","authors":"Shuwei Gao, Yanqiu Wei, Chen Li, Bingbing Xie, Xinran Zhang, Ye Cui, Huaping Dai","doi":"10.1152/ajpcell.00374.2024","DOIUrl":"10.1152/ajpcell.00374.2024","url":null,"abstract":"<p><p>Idiopathic pulmonary fibrosis (IPF) is a progressive and degenerative interstitial lung disease characterized by complex etiology, unclear pathogenesis, and high mortality. Long noncoding RNAs (lncRNAs) have been identified as key regulators in modulating the initiation, maintenance, and progression of pulmonary fibrosis. However, the precise pathological mechanisms through which lncRNAs are involved in IPF remain limited and require further elucidation. A novel lncABCE1-5 was identified as significantly decreased by an ncRNA microarray analysis in our eight IPF lung samples compared with three donor tissues and validated by quantitative real-time polymerase chain reaction (qRT-PCR) analysis in clinical lung samples. To investigate the biological function of ABCE1-5, we performed loss- and gain-of-function experiments in vitro and in vivo. LncABCE1-5 silencing promoted A549 cell migration and A549 and bronchial epithelial cell line (BEAS-2B) cell apoptosis while enhancing the expression of proteins associated with extracellular matrix deposition, whereas overexpression of ABCE1-5 partially attenuated transforming growth factor-beta (TGF-β)-induced fibrogenesis. Forced ABCE1-5 expression by intratracheal injection of adeno-associated virus 6 revealing the antifibrotic effect of ABCE1-5 in bleomycin (BLM)-treated mice. Mechanistically, RNA pull-down (RPD)-mass spectrometry and RNA immunoprecipitation assay demonstrated that ABCE1-5 directly binds to keratin14 (krt14) sequences, potentially impeding its expression by perturbing mRNA stability. Furthermore, decreased ABCE1-5 levels can promote krt14 expression and enhance the phosphorylation of both mTOR and Akt; overexpression of ABCE1-5 in BLM mouse lung tissue significantly attenuated the elevated levels of p-mTOR and p-AKT. Knockdown of krt14 reversed the activation of mTOR signaling mediated by ABCE1-5 silencing. Collectively, the downregulation of ABCE1-5 mediated krt14 activation, thereby activating mTOR/AKT signaling, to facilitate pulmonary fibrosis progression in IPF.<b>NEW & NOTEWORTHY</b> In the present study, our data first reveal that a novel lncRNA ABCE1-5 could inhibit pulmonary fibrosis through interacting with krt14 and negative regulation of its expression, and indicated ABCE1-5 also regulates the phosphorylation of mTOR and Akt, thus acting on extracellular matrix remodeling in lung fibrosis procession. These results suggest that novel molecules within the ABCE1-5-krt14-mTOR axis may serve as potential candidates for clinical application in IPF.</p>","PeriodicalId":7585,"journal":{"name":"American journal of physiology. Cell physiology","volume":" ","pages":"C1487-C1500"},"PeriodicalIF":5.0,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143668864","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}