American journal of physiology. Cell physiology最新文献

{"title":"CFTR High Expresser BEST4+ cells are pH-sensing neuropod cells: new implications for intestinal physiology and Cystic Fibrosis disease.","authors":"Diego C Dos Reis, Jason Jin, Anderson Santos, Parinaz Dastoor, Caroline Muiler, Eleanor Zagoren, Martin Donnelley, David Parsons, Patricia Cmielewski, Nicole Reyne, Alexandra McCarron, Zachary Smith, Kaelyn Sumigray, Nadia A Ameen","doi":"10.1152/ajpcell.00082.2025","DOIUrl":"https://doi.org/10.1152/ajpcell.00082.2025","url":null,"abstract":"<p><p>Single-cell RNA sequencing (scRNA-seq) studies identified a novel subpopulation of epithelial cells along the rostrocaudal axis of human intestine specifically marked by bestrophin 4 (BEST4) that are enriched for genes regulating pH, GPCR acid-sensing receptors, satiety, cGMP signaling, HCO3^- secretion, ion transport, neuropeptides, and paracrine hormones. Interestingly, BEST4+ cells in the proximal small intestine express CFTR but have not been widely linked to the previously described CFTR High Expresser Cell (CHE) subpopulation in rat and human intestine. ScRNA-seq studies in rat jejunum identified CHEs and a gene expression profile consistent with human small intestinal BEST4+ and neuropod cells. Protein immunolocalization confirmed that CHEs express CFTR, BEST4, neuropod proteins, high levels of intracellular uroguanylin (UGN), guanylyl cyclase-C (GC-C), and the proton channel otopetrin 2 (OTOP2), and display long basal processes connecting to neurons, confirming that Best4+ cells in the proximal small intestine are CHEs. OTOP2, GC-C, and CFTR traffic robustly into the apical domain of CHEs in response to acidic luminal conditions, indicating their roles in luminal pH regulation. In the ΔF508 cystic fibrosis (CF) rat jejunum, the loss of apical CFTR did not affect BEST4 protein expression in CHEs. However, there was an increased abundance of CHE cells in the ΔF508 rat jejunum compared to wild-type animals. Furthermore, ΔF508 rat CHEs expressed higher levels of GC-C at the apical domain compared to wild-type. These data implicate CHEs in intestinal CF disease pathogenesis.</p>","PeriodicalId":7585,"journal":{"name":"American journal of physiology. Cell physiology","volume":" ","pages":""},"PeriodicalIF":4.7,"publicationDate":"2025-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145172191","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":"Isolation of functional lysosomes from skeletal muscle.","authors":"Thulasi Mahendran, Anastasiya Kuznyetsova, Neushaw Moradi, David A Hood","doi":"10.1152/ajpcell.00471.2025","DOIUrl":"https://doi.org/10.1152/ajpcell.00471.2025","url":null,"abstract":"<p><p>Lysosomes are membrane-bound organelles responsible for the degradation of damaged or dysfunctional cellular components, including mitochondria. Their acidic internal environment and the presence of an array of hydrolytic enzymes facilitate the efficient breakdown of macromolecules such as proteins, lipids, and nucleic acids. Mitochondria play a critical role in maintaining skeletal muscle homeostasis to meet the energy demands under physiological and pathological conditions. Mitochondrial quality control within skeletal muscle during processes such as exercise, disuse, and injury is regulated by mitophagy, where dysfunctional mitochondria are targeted for lysosomal degradation. The limited understanding of quality control mechanisms in skeletal muscle necessitates the need for isolating intact lysosomes to assess organelle integrity and the degradative functions of hydrolytic enzymes. Although several methods exist for lysosome isolation, the complex structure of skeletal muscle makes it challenging to obtain relatively pure and functional lysosomes due to the high abundance of contractile proteins. Here we describe a method to isolate functional lysosomes from small amounts of mouse skeletal muscle tissue, preserving membrane integrity. We also describe functional assays that allow direct evaluation of lysosomal enzymatic activity and we provide data indicating reduced lysosomal degradative activity in lysosomes from aging muscle. We hope that this protocol provides a valuable tool to advance our understanding of lysosomal biology in skeletal muscle, supporting investigations into lysosome-related dysfunction in aging, disease, and exercise adaptations.</p>","PeriodicalId":7585,"journal":{"name":"American journal of physiology. Cell physiology","volume":" ","pages":""},"PeriodicalIF":4.7,"publicationDate":"2025-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145111739","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":"Molecular Signaling in Biomaterial-induced Foreign Body Response: Current Perspectives.","authors":"Suneha G Rahaman, Mohammad I Khan, Karunakaran R Sankaran, Shaik O Rahaman","doi":"10.1152/ajpcell.00595.2025","DOIUrl":"https://doi.org/10.1152/ajpcell.00595.2025","url":null,"abstract":"<p><p>The foreign body response (FBR) is an inevitable host response to implanted materials, initiated by tissue injury and marked by a cascade of inflammatory and fibrotic processes. Following implantation, local tissue damage triggers acute inflammation, characterized by immune cell recruitment and activation. Over time, this response advances to a chronic fibrotic phase marked by dense extracellular matrix deposition and fibrous capsule formation, which can encapsulate and, in some cases, functionally isolate the implant. Both the early inflammatory and late fibrotic stages of FBR can severely impair the performance and longevity of implants. FBR is governed by a dynamic and multifaceted network of molecular signaling pathways, cellular mechanosensing mechanisms, and intercellular communication. Despite its clinical significance, the molecular underpinnings of FBR remain incompletely defined. A deeper molecular understanding is critical for the rational design of next-generation biomaterials that mitigate adverse host responses and improve biocompatibility. In this review, we provide the first comprehensive overview of the current knowledge of the molecular events driving FBR, with the goal of informing strategies for therapeutic modulation and biomaterial innovation.</p>","PeriodicalId":7585,"journal":{"name":"American journal of physiology. Cell physiology","volume":" ","pages":""},"PeriodicalIF":4.7,"publicationDate":"2025-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145111769","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":"Multifaceted role of AMPK in autophagy: more than a simple trigger?","authors":"Milos Mandic, Maja Misirkic Marjanovic, Kristina Janjetovic, Mihajlo Bosnjak, Ljubica Harhaji-Trajkovic, Vladimir Trajkovic, Ljubica Vucicevic","doi":"10.1152/ajpcell.01058.2024","DOIUrl":"https://doi.org/10.1152/ajpcell.01058.2024","url":null,"abstract":"<p><p>AMP-activated protein kinase (AMPK) is a key sensor and regulator of intracellular energy balance. During energy stress, AMPK helps restore cellular ATP levels by preventing anabolic and promoting catabolic processes, such as autophagy. AMPK activates autophagy both post-translationally and transcriptionally, by suppressing the mechanistic target of rapamycin complex 1 activity and stimulating the activation of unc-51 like autophagy activating kinase (ULK), autophagosome-lysosome fusion, and expression of autophagy-related genes. Recent research, however, suggests an unexpected role of AMPK in energy stress, where AMPK inhibits ULK and suppresses ATP-consuming autophagic response, possibly to save energy and maintain the autophagic machinery for subsequent activation once the stress subsides. The present review elucidates this dual nature of AMPK in autophagy regulation while highlighting its molecular mechanisms and importance for therapeutic approaches involving AMPK modulation.</p>","PeriodicalId":7585,"journal":{"name":"American journal of physiology. Cell physiology","volume":" ","pages":""},"PeriodicalIF":4.7,"publicationDate":"2025-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145068890","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":"Local injection of particles for retinoic acid drug delivery improves muscle structure and modulates inflammation in mice recovering from cast immobilization.","authors":"Candice V Cheung, Regina A Searcy, Kidochukwu J Atube, Nicholas A Colonna, Kelsey E Krusen, Kate J Coppage, Khufu M Holly, R Paul Ward Pratz, Jesse H Fournier, Vitali Sikirzhytski, Ashley J Smuder, R Michael Gower","doi":"10.1152/ajpcell.00097.2025","DOIUrl":"https://doi.org/10.1152/ajpcell.00097.2025","url":null,"abstract":"<p><p>Disuse muscle atrophy secondary to acute illness or injury prolongs recovery and increases risk of permanent disability as a result of reduced muscle strength and myofiber damage upon reambulation. However, there are no pharmacotherapies to support muscle growth and repair following prolonged immobility. We propose that all-trans retinoic acid (ATRA) may support recovery of atrophied muscle via modulation of satellite cells and macrophages. Clinical application of ATRA is hindered by solubility, stability, and the need for high systemic doses. Therefore, in the current study, we developed poly(lactide-co-glycolide) (PLG) particles for local injection and extended release of ATRA (ATRA-PLG) and investigated the impact of ATRA-PLG on muscle recovery from disuse atrophy in adult mice following 10 days of hindlimb cast immobilization. A single administration of ATRA-PLG to the facia surrounding the calf muscle, at the time of cast removal, accelerates recovery of soleus muscle cross-sectional area. This is associated with decreased tissue damage, increased expression of macrophage scavenger receptors CD206 and CD163, and decreased CD68 and IL-6. Meanwhile, markers of muscle repair and growth are weakly impacted by ATRA-PLG. The data suggest that ATRA-PLG modulation of macrophages may limit inflammation and secondary injury to the atrophied muscle during the early stages of recovery, which then requires a lower repair response, and this translates to accelerated recovery of cross-sectional area. Our findings lay the foundation for future investigations of ATRA-PLG in populations that exhibit incomplete recovery from atrophy and dysregulated macrophage function, such as the elderly.</p>","PeriodicalId":7585,"journal":{"name":"American journal of physiology. Cell physiology","volume":" ","pages":""},"PeriodicalIF":4.7,"publicationDate":"2025-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145068799","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":"Vascular ageing impairs active modulation of murine aortic stiffness by smooth muscle cells.","authors":"Koen W F van der Laan, Cédric H G Neutel, Margarita G Pencheva, Callan D Wesley, Dustin N Krüger, Casper G Schalwijk, Guido R Y De Meyer, Wim Martinet, Koen D Reesink, Tammo Delhaas, Alessandro Giudici, Pieter-Jan Guns, Bart Spronck","doi":"10.1152/ajpcell.00387.2025","DOIUrl":"https://doi.org/10.1152/ajpcell.00387.2025","url":null,"abstract":"<p><p><b>Background</b> Ageing causes changes to arterial contractility and tissue microstructure, resulting in arterial stiffening, a strong risk factor for cardiovascular diseases. Because the interaction between these effects is largely unexplored, this study aims to investigate how ageing-induced changes in contractility and wall constituent microstructure impact arterial biomechanics in murine aortas. <b>Methods</b> Vasoreactive responses of thoracic descending aortas of adult (5-months-old, <i>n</i>=5) and old (24-months-old, <i>n</i>=5) C57Bl/6J mice to phenylephrine, N-Ω-Nitro-L-arginine methyl ester (L-NAME), and sodium nitroprusside were measured under dynamic pressurization conditions. Whole-vessel and individual-constituent biaxial viscoelastic properties were characterized during contraction and relaxation while mimicking physiological dynamic loading conditions. In addition, elastin fibers, collagen fibers, and smooth muscle nuclei microstructural organization and morphological properties were quantified in pressurized aortas using two-photon laser scanning microscopy. <b>Results</b> Compared to adult mice, aortas of old mice displayed thicker walls but similar pressure-diameter behaviors in the absence of contraction. Vasoconstriction in aortas of adult mice 1) significantly increased wall thickness, 2) reduced pulse wave velocity at physiologically high pressure ranges, 3) reduced circumferential and axial stresses and stiffnesses, and 4) altered constituent load bearing. Conversely, aortas of old mice exhibited reduced contractility, altered vasoreactive responses, and reduced cell density. As a result, they were uncapable to alter any of their biomechanical properties through vasoconstriction. <b>Conclusion</b> Vasoconstriction enables modulation of axial and circumferential stresses and stiffnesses in the adult mouse aorta. With ageing, this modulatory capacity was impaired.</p>","PeriodicalId":7585,"journal":{"name":"American journal of physiology. Cell physiology","volume":" ","pages":""},"PeriodicalIF":4.7,"publicationDate":"2025-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145051506","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":"Amino Acid Metabolism in Cancer Cachexia and Chemotherapy Myotoxicity.","authors":"Meghan V McCue, David A MacLean","doi":"10.1152/ajpcell.00085.2025","DOIUrl":"https://doi.org/10.1152/ajpcell.00085.2025","url":null,"abstract":"<p><p>Cancer induced skeletal muscle wasting (cachexia) is responsible for over 20% of cancer related deaths, yet much about the pathophysiology of the condition remains unknown. Importantly, cancer cachexia does not seem wholly responsive to traditional anabolic stimuli such as nutritional interventions. It is possible that tumours directly or indirectly target skeletal muscle for their dynamic and abundant pool of amino acids that can be reliably used by tumours to supplement energy production and biomass synthesis. Therefore, understanding how the presence of a tumour alters circulating and tissue level amino acid pools could provide valuable insight into tumour induced muscle wasting. The purpose of this review was to examine the current body of research that has studied amino acids in the context of cancer cachexia, to better understand how amino acids behave during the development of cancer, cachexia, and various cancer chemotherapies. Distinct heterogeneity was observed in the behaviour of amino acids when comparing weight stable vs. cachectic patients with cancer, and there may be important temporal considerations based on rhythmic changes in amino acid turnover and mealtimes. Overall, there was very little consistency in the reported fluctuations of amino acids from study to study, suggesting there may be heterogenous pathophysiology based on tumour type, stage, and patient age and co-morbidities. Further work is required to characterize longitudinal changes in amino acid metabolism with consideration for these factors. Enhancing our understanding of amino acid metabolism during cancer cachexia could provide opportunities for advancement in practical methodologies in cachexia research and treatment strategies.</p>","PeriodicalId":7585,"journal":{"name":"American journal of physiology. Cell physiology","volume":" ","pages":""},"PeriodicalIF":4.7,"publicationDate":"2025-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145032566","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":"Deletion of ABIN1-LIR motifs impairs hepatic lipid homeostasis and mitophagy via AMPK-TFEB axis in mice.","authors":"Lisa Sophie Huber, Rosetta Merline, Jinyang Zeng-Brouwers, Rajkumar Vutukuri, Nico Kraus, Cristina Ortiz, Stefan Guenther, Eva Miriam Buhl, Lisa Hahnefeld, Robert Gurke, Julia Bein, Madina Karimova, Patrick Wurzel, Peter Boor, Christoph Welsch, Peter Wild, Josef Pfeilschifter, Donat Kögel, Malgorzata Wygrecka, Jonel Trebicka, Rafal Bartoszewski, Ivan Dikic, Liliana Schaefer","doi":"10.1152/ajpcell.00544.2025","DOIUrl":"https://doi.org/10.1152/ajpcell.00544.2025","url":null,"abstract":"<p><p>The A20 binding inhibitor of nuclear factor-kappa B (NF-κB)-1 (ABIN-1) serves as a ubiquitin sensor and autophagy receptor, crucial for modulating inflammation and cell death. Our previous in vitro investigation identified the LC3-interacting region (LIR) motifs 1 and 2 of ABIN-1 as key mitophagy regulators. This study aimed to explore the in vivo biological significance of ABIN1-LIR domains using a novel CRISPR-engineered ABIN1-ΔLIR1/2 mouse model, which lacks both LIR motifs. Comprehensive morphological, serum, and tissue histochemical analyses revealed increased body, fat, and liver weights, altered serum and hepatic lipid profiles, and substantial hepatic lipid droplet accumulation, indicative of altered hepatic lipid metabolism, dyslipidemia, and hepatic steatosis in ABIN1-ΔLIR1/2 mice. Transcriptomic, metabolomic, and lipidomic analyses indicated dysregulated hepatic mitochondrial metabolism, favoring lipogenesis. Mechanistically, LIR1/2 deletion inhibited the expression and activity of transcription factor EB (TFEB) and AMP-activated protein kinase β1 (AMPKβ1), resulting in compromised autophagy and lipophagy. ABIN1 interacted with TFEB and colocalization was observed in both the cytoplasmic and nuclear compartments of hepatocytes. Impaired mitophagy was evidenced by the decreased expression of parkin and optineurin, along with increased levels of mitochondrial cytochrome c oxidase subunit II. These findings were corroborated by liver biopsies of patients with metabolic dysfunction-associated steatotic liver disease. Thus, this study underscores the functional role of ABIN1-LIR motifs in modulating the ABIN1-AMPK-TFEB axis, which is critical for mitochondria-associated lipid metabolism and mitophagy, offering insights into the mechanistic pathways contributing to the pathogenesis of steatosis-associated liver diseases with potential therapeutic implications.</p>","PeriodicalId":7585,"journal":{"name":"American journal of physiology. Cell physiology","volume":" ","pages":""},"PeriodicalIF":4.7,"publicationDate":"2025-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145022669","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":"Early Regulation and Alternative Splicing Dynamics in Glucocorticoid Muscle Atrophy Revealed by Temporal Omics in C2C12 Myotubes.","authors":"Suzuka Nakagawa, Aristotelis Misios, Oliver Popp, Philipp Mertins, Ernst Jarosch, Jens Fielitz, Thomas Sommer","doi":"10.1152/ajpcell.00518.2025","DOIUrl":"https://doi.org/10.1152/ajpcell.00518.2025","url":null,"abstract":"<p><p>Skeletal muscle atrophy and weakness are major contributors to morbidity, prolonged recovery, and long-term disability across a wide range of diseases. Atrophy is caused by breakdown of sarcomeric proteins resulting in loss of muscle mass and strength. Molecular mechanism underlying the onset of muscle atrophy and its progression have been analysed in patients, mice, and cell culture but the complementarity of these model systems remains to be explored. Here, we applied deep-coverage transcriptomic and proteomic profiling for an updated view on dynamic changes during dexamethasone-induced atrophy in the widely used murine skeletal muscle cell line C2C12. Comparison with published mouse data confirmed that muscle differentiation is well recapitulated in C2C12 myotubes. Under dexamethasone treatment, this model was particularly suited to capture early atrophy events. We additionally identified alterations in mitochondrial gene expression and differential alternative splicing events during early-stage myotube atrophy. This dataset complements existing <i>in vivo</i> data and provides novel insights into the regulatory processes during skeletal muscle wasting.</p>","PeriodicalId":7585,"journal":{"name":"American journal of physiology. Cell physiology","volume":" ","pages":""},"PeriodicalIF":4.7,"publicationDate":"2025-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145022710","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":"The IL-33/ST2/ILC2 pathway in kidney disease: balancing inflammation, fibrosis, and repair.","authors":"Yasunari Matsuzaka, Masayuki Iyoda","doi":"10.1152/ajpcell.00405.2025","DOIUrl":"10.1152/ajpcell.00405.2025","url":null,"abstract":"<p><p>Group 2 innate lymphoid cells (ILC2s) are tissue-resident immune cells that respond rapidly to epithelial-derived cytokines such as interleukin (IL)-33, producing type 2 cytokines including IL-5 and IL-13. Although ILC2s are well recognized for their roles in regulating inflammation and tissue remodeling in barrier organs, their functions in the kidney have only recently gained attention. In this review, we summarize the localization, activation, and effector functions of ILC2s in the kidney and explore their immunoregulatory interactions with macrophages, particularly in promoting M2 polarization. We further provide an overview of the therapeutic relevance of the IL-33/ST2/ILC2 axis in renal pathology, organizing current findings across models of acute kidney injury (AKI), chronic kidney disease (CKD), and glomerulonephritis (GN). ILC2s are primarily distributed in the perivascular tubulointerstitial regions of both the renal cortex and outer medulla, where they exert anti-inflammatory and antifibrotic effects through cytokine-mediated mechanisms. Importantly, recent studies suggest that the outcomes of IL-33-mediated interventions are highly context-dependent, influenced by factors such as dosage, disease phase, and temporal dynamics. A comprehensive understanding of the IL-33/ST2/ILC2 axis may offer new insights into immune modulation and tissue protection strategies for kidney diseases.</p>","PeriodicalId":7585,"journal":{"name":"American journal of physiology. Cell physiology","volume":" ","pages":"C718-C725"},"PeriodicalIF":4.7,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144706043","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}