American journal of physiology. Cell physiology最新文献

{"title":"Fluid restriction enhances mitochondrial stress in peripheral blood mononuclear cells following high-volume resistance exercise in health young males.","authors":"Hui-Ying Luk, Casey R Appell, Nigel C Jiwan, Heather L Vellers, Yasuki Sekiguchi, Danielle E Levitt","doi":"10.1152/ajpcell.00859.2025","DOIUrl":"10.1152/ajpcell.00859.2025","url":null,"abstract":"<p><p>Exercising under dehydrated conditions is common among physically active individuals, yet its impact on immune cell mitochondrial quality control, oxidative stress and inflammatory signaling, and systemic inflammatory mediators remains poorly defined. This study investigated mitochondrial quality control and systemic inflammatory responses to high-volume resistance exercise (HVRE) under hydrated (HYD) and dehydrated (DEH) conditions in 10 young men (21 ± 1 yr, 175 ± 6 cm, 76.9 ± 10.5 kg, 18.5 ± 6.3% fat). Participants completed two identical HVRE sessions following either normal hydration or 24-h fluid restriction. Peripheral blood mononuclear cells (PBMCs) collected before (PRE) and at 1 h and 3 h post-HVRE were analyzed for proteins related to mitochondrial quality control (PINK1, Parkin, DRP1, p-DRP1^S616, and MFN2), oxidative stress and inflammatory signaling (p-NF-κB^S536, NF-κB, SOD2, and H₂O₂), autophagy machinery and degradation (LC3-I, LC3-II, p62, and cathepsin-L), and blood samples for systemic inflammatory mediators (IL-6, TNF-α, CRP, and H₂O₂). Significant time × condition interaction effects revealed that LC3-II/I was greater in DEH than HYD at PRE and 3 h. In DEH, LC3-II/I returned to PRE levels at 3 h, whereas in HYD, it was greatest at 3 h. PINK1 was greater at 1 h and 3 h, and pDRP1^S616 was greater at 3 h in DEH than HYD. Also, PINK1 and pDRP1^S616 were greatest at 3 h post-HVRE in DEH. Lastly, significant condition main effects revealed greater MFN2, p62, LC3-II, and H₂O₂ in PBMCs and greater IL-6 and CRP in serum in DEH than in HYD. These results provide novel evidence that 24 h of fluid restriction before metabolically demanding resistance exercise activates mitochondrial quality control in PBMCs and elevates systemic inflammatory mediators.<b>NEW & NOTEWORTHY</b> This study examined how 24-h fluid restriction affects mitochondrial stress and inflammatory responses in peripheral blood mononuclear cells (PBMCs) after high-volume resistance exercise in young men. Dehydration increased markers of mitophagy (PINK1 and p-DRP1^S616), autophagosome formation (LC3-II and p62), and oxidative stress (H₂O₂), while systemic IL-6 and CRP were elevated compared with euhydration. Findings suggest dehydration amplifies mitochondrial stress and proinflammatory signaling, highlighting the importance of proper hydration during exercise and its implications on cellular homeostasis.</p>","PeriodicalId":7585,"journal":{"name":"American journal of physiology. Cell physiology","volume":" ","pages":"C1631-C1646"},"PeriodicalIF":5.4,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147832305","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 role of glycolysis in inflammation.","authors":"Ethan T Dehantschutter, Cormac T Taylor","doi":"10.1152/ajpcell.00113.2026","DOIUrl":"10.1152/ajpcell.00113.2026","url":null,"abstract":"<p><p>A characteristic feature of inflamed tissue is hypoxia, which arises from elevated oxygen consumption and impaired perfusion. Inflammation is accompanied by metabolic reprogramming enabling immune and nonimmune cells to meet increased bioenergetic and biosynthetic demands. Glycolysis is among the most ancient and fundamental metabolic pathways in biology. Hypoxia reduces mitochondrial oxidative phosphorylation, driving cells toward a reliance on glycolysis to sustain ATP production. This requires an increase in flux through the glycolytic pathway, which is mediated through rapid allosteric regulation of glycolytic enzymes, transcriptional upregulation of glucose transporters and glycolytic enzymes, and the formation of glycolytic enzyme complexes. In immune cells such as macrophages, neutrophils, and lymphocytes, enhanced glycolytic flux determines effector functions, including, but not limited to, cytokine production, phagocytosis, migration, and antimicrobial activity, as well as maintaining bioenergetic homeostasis. Similarly, nonimmune cells within inflamed tissues, including epithelial cells and stromal cells, utilize glycolysis to influence barrier function, tissue remodeling, and inflammation. In this review, we summarize our current understanding of how hypoxia drives glycolytic reprogramming during inflammation, examine the cell-type-specific impact of this, and discuss the therapeutic potential of targeting glycolytic pathways for inflammatory diseases.</p>","PeriodicalId":7585,"journal":{"name":"American journal of physiology. Cell physiology","volume":" ","pages":"C1669-C1691"},"PeriodicalIF":5.4,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147855700","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":"Moderate forced running exercise induces cartilage adaptation but exacerbates the molecular cartilage phenotype of type IX collagen knockout mice.","authors":"Miriam Weyers, Thomas Li, Maren Dreiner, Daniela Mählich, Charlotte Lorenz, Luisa de Roy, Paola Zigrino, Lin Han, Bent Brachvogel, Frank Zaucke, Anja Niehoff","doi":"10.1152/ajpcell.00959.2025","DOIUrl":"10.1152/ajpcell.00959.2025","url":null,"abstract":"<p><p>Mechanical loading is essential for the assembly and maintenance of the articular cartilage extracellular matrix (ECM), whereas alterations in ECM composition profoundly affect cartilage mechanics and function. Type IX collagen is a heterotrimeric fibril-associated collagen with interrupted triple helices (FACIT) that is covalently linked to type II collagen. It restricts lateral fibril growth and mediates interactions with other ECM components. Although type IX collagen expression is mechanosensitive and implicated in cartilage mechanotransduction, its precise functional role is not yet fully understood. This study investigated the combined effects of type IX collagen deficiency and moderate mechanical loading on articular and growth plate cartilage. Twelve-week-old female wild-type (WT) and <i>Col9a1</i>^-/- mice were randomly assigned to control (CON) or forced running exercise (EXE) groups (<i>n</i> = 10-12 per group). EXE animals underwent treadmill training for 6 wk (20% incline, 18 m/min, 40 min/day, 5 days/wk). Type IX collagen deficiency resulted in an abnormal growth plate architecture and a reduction of all matrilins and cartilage oligomeric matrix protein (COMP) in articular cartilage. Moderate forced running exercise induced a significant increase (<i>P</i> < 0.05) in cartilage thickness at the lateral femoral condyle and altered ECM composition in <i>Col9a1</i>^-/- mice, without evidence of cartilage degeneration. WT mice showed no comparable structural changes. In conclusion, moderate mechanical loading elicits localized, nondegenerative, structural and molecular adaptations in articular cartilage and only modestly modulates the cartilage phenotype associated with type IX collagen deficiency. These findings suggest a limited, yet context-dependent role of type IX collagen in cartilage mechanoadaptation.<b>NEW & NOTEWORTHY</b> Moderate forced running exercise only slightly enhances the cartilage phenotype in aging female type IX collagen knockout mice and induces local, nondegenerative, structural and molecular adaptations in the articular cartilage ECM. Alterations in the cartilage phenotype do not depend on the age of the mice.</p>","PeriodicalId":7585,"journal":{"name":"American journal of physiology. Cell physiology","volume":" ","pages":"C1704-C1720"},"PeriodicalIF":5.4,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147969628","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":"Rethinking holocrine secretion: functional logic in lipid-producing epithelia.","authors":"Marlon R Schneider","doi":"10.1152/ajpcell.00191.2026","DOIUrl":"10.1152/ajpcell.00191.2026","url":null,"abstract":"<p><p>Holocrine secretion is typically described as an exception among glandular strategies, distinguished by cell disintegration and release of cellular fragments rather than vesicular contents. Yet this description treats holocrine glands primarily as anatomical curiosities and leaves their underlying biological logic largely unexplored. Here, we propose that holocrine secretion can instead be understood as a differentiation program that couples lipid accumulation, terminal differentiation, and cell elimination. This design supports surface barrier function and points toward differentiation-based approaches for controlled epithelial cell removal.</p>","PeriodicalId":7585,"journal":{"name":"American journal of physiology. Cell physiology","volume":" ","pages":"C1647-C1650"},"PeriodicalIF":5.4,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147855567","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":"Divergent mitochondrial stressors elicit specific retrograde signaling pathways in muscle myotubes.","authors":"Klaudia Sztolsztener, Thulasi Mahendran, David A Hood","doi":"10.1152/ajpcell.00167.2026","DOIUrl":"10.1152/ajpcell.00167.2026","url":null,"abstract":"<p><p>Protein homeostasis is critical for mitochondrial function and is maintained by proteases and chaperones that respond to stress and mediate adaptive changes such as the mitochondrial unfolded protein response (UPRmt), the integrated stress response (ISR), and antioxidant signaling. However, the mechanisms by which stressors regulate these retrograde responses remains uncharacterized in muscle. Thus, we examined the effect of mitochondrial stressors on the activation of these pathways in myoblasts and differentiated myotubes. Cells were exposed to either <i>1</i>) 2-Cyano-3,12-dioxooleana-1,9(11)-dien-28-oic acid (CDDO), a LonP1 protease inhibitor, <i>2</i>) gamitrinib-triphenylphosphonium (GTPP), an HSP90 chaperone inhibitor, <i>3</i>) carbonyl cyanide <i>m</i>-chlorophenyl hydrazone (CCCP), an energetic uncoupler, or <i>4</i>) MitoBloCK-10 (MB-10), an inhibitor of protein import, and responses were compared with those induced by acute contractile activity (ACA). LonP1 inhibition activated activating transcription factor 4 (ATF4) and Nrf2 signaling, increased mitochondrial chaperones, and resulted in protein aggregation without elevating reactive oxygen species (ROS). In contrast, blocking HSP90 led to increases in mitochondrial ROS and activation of C/EBP homologous protein (CHOP), indicating protein homeostasis-related stress with limited antioxidant signaling. ACA elicited responses similar to the inhibition of LonP1, including the activation of ATF4 and Nrf2, increased UPRmt markers, and a redox balance. Although CCCP and MB-10 both impaired protein import, they activated distinct downstream responses. CCCP resulted in ISR activation, whereas MB-10 induced Nrf2-mediated antioxidant responses. Together, these findings show that the type of mitochondrial stress determines the direction of the retrograde signaling pathways between protein homeostasis and redox signaling in muscle cells, and they provide insights on how muscle coordinates signaling pathways as part of mitochondrial adaptations to contractile activity.<b>NEW & NOTEWORTHY</b> This study investigates how different mitochondrial stressors activate distinct cellular signaling pathways in skeletal muscle cells. It examines how cells maintain a balance between protein homeostasis and oxidative stress when mitochondrial proteases, chaperones, and protein import are inhibited, and during acute contractile activity. The findings from this study provide key insights into mitochondrial protein homeostasis, stress signaling, and muscle adaptation mechanisms highlighting that downstream adaptive responses depend on the type of stressors.</p>","PeriodicalId":7585,"journal":{"name":"American journal of physiology. Cell physiology","volume":" ","pages":"C1721-C1736"},"PeriodicalIF":5.4,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147925657","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":"Discovery of Kv3.1 channel inhibitors reveals VU0521426 as a state-dependent inactivator preferentially active against pathogenic gain-of-function mutants.","authors":"Rahul U Chandrappa, Vaishali Satpute Janve, Emily L Days, Jerod S Denton","doi":"10.1152/ajpcell.00239.2026","DOIUrl":"10.1152/ajpcell.00239.2026","url":null,"abstract":"<p><p>Kv3.1 voltage-gated potassium channels play a critical role in regulating neuronal excitability, and dysregulation driven by gain-of-function (GoF) mutations has been implicated in neurological disease. Although Kv3.1 potentiators have been at the forefront of drug development as a means to enhance neuronal firing, progress towards small-molecule Kv3.1 inhibitors has been limited. Here, we address this gap with the discovery of novel and structurally diverse Kv3.1 channel inhibitors identified through a high-throughput screening of over 50,000 compounds. Among these, VU426 emerged as the most potent compound with an IC₅₀ of 4.3 μM. VU426 induces pronounced, state-dependent inhibition of outward K⁺ current with sustained depolarization, indicating stabilization of an inactivated channel conformation accessed from the open state. Functional characterization of four GoF mutations (V425M, M430I, V432M, and V434L) in the S6 pore lining domain demonstrated that VU426 exhibits 1.5- to 5-fold enhanced potency toward pathogenic GoF Kv3.1 mutants relative to wild-type channels. Automated patch clamp electrophysiological studies revealed that V432M and V434L mutations embedded deep in the S6 domain had the greatest sensitivity to VU426. Despite its potency, VU426 exhibited limited selectivity for Kv3.1 over related Kv channels. Together, these findings identify novel Kv3.1 inhibitors and highlight a pharmacological strategy for targeting clinically identified pathogenic variants.<b>NEW & NOTEWORTHY</b> This study identifies the first structurally diverse collection of small-molecule inhibitors of Kv3.1 potassium channels, highlighting VU426 as a moderately potent, state-dependent inactivator. Notably, VU426 displays enhanced potency against multiple pathogenic gain-of-function Kv3.1 mutants, revealing a mechanism-based strategy for selectively targeting disease-associated channel variants.</p>","PeriodicalId":7585,"journal":{"name":"American journal of physiology. Cell physiology","volume":" ","pages":"C1788-C1799"},"PeriodicalIF":5.4,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13270922/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147947571","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":"β-Hydroxybutyrate attenuates bronchial smooth muscle proinflammatory cytokine production and contraction.","authors":"V Amanda Fastiggi, Madeleine M Mank, Matthew A Caporizzo, Matthew E Poynter","doi":"10.1152/ajpcell.00169.2026","DOIUrl":"10.1152/ajpcell.00169.2026","url":null,"abstract":"<p><p>Asthma is a chronic respiratory condition characterized by airway inflammation, remodeling, and hyperresponsiveness to triggers that lead to airway constriction and impaired airflow. Bronchial smooth muscle (BSM) plays a central role in these processes by constricting the airways and producing proinflammatory cytokines in response to environmental triggers, allergens, and cytokines. Although current therapies, including bronchodilators, corticosteroids, and biologics, effectively treat many patients, additional strategies are needed for difficult-to-treat asthma. Emerging evidence suggests that therapeutic ketosis, achieved through dietary interventions or exogenous ketone supplementation, may reduce airway hyperresponsiveness and inflammation. Classically known as metabolic fuels, ketone bodies also signal through cell-surface receptors and transporters to elicit their activities. Increased ketone body levels in vivo, such as during weight loss or caloric restriction, correlate with improved asthma symptoms, reduced oxidative stress, and decreased inflammation. Here, we investigated the predominant ketone body, β-hydroxybutyrate (BHB), as a potential modulator of BSM function. Using human bronchial smooth muscle cells in vitro, we found that BHB suppresses IL-1β-induced proinflammatory cytokine production and attenuates histamine-induced contraction through a mechanism involving activation of the free fatty acid receptor 3 (FFAR3). In mouse precision-cut lung slices (PCLS) ex vivo, we demonstrated that both BHB and an FFAR3 agonist reduce histamine-induced airway narrowing and epithelial cellular extrusion. Collectively, these findings identify BSM and FFAR3 as cellular targets of therapeutic ketosis and support BHB as a potential beneficial agent for mitigating inflammation and bronchoconstriction in asthma.<b>NEW & NOTEWORTHY</b> Asthma is characterized by airway inflammation and bronchoconstriction, with aberrant bronchial smooth muscle function contributing to disease severity. Therapeutic ketosis, achieved through a ketogenic diet or exogenous ketone supplementation, attenuates airway inflammation and bronchial hyperresponsiveness. Using bronchial smooth muscle cells and precision-cut lung slices, we demonstrate that the ketone body β-hydroxybutyrate (BHB) suppresses IL-1β-induced proinflammatory cytokine production and histamine-evoked bronchoconstriction via activation of the free fatty acid receptor FFAR3.</p>","PeriodicalId":7585,"journal":{"name":"American journal of physiology. Cell physiology","volume":" ","pages":"C1561-C1573"},"PeriodicalIF":5.4,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13224875/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147759940","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":"Dietary supplementation with ursolic acid preserves skeletal muscle mass and strength in mouse models of cancer cachexia.","authors":"Jeremy B Ducharme, Scott M Ebert, Miles E Cameron, Martin M Schonk, Chandler S Callaway, Andrew C D'Lugos, John J Talley, Sarah M Judge, Christopher M Adams, Andrew R Judge","doi":"10.1152/ajpcell.00159.2026","DOIUrl":"10.1152/ajpcell.00159.2026","url":null,"abstract":"<p><p>Skeletal muscle atrophy is a devastating and defining feature of cancer cachexia that reduces quality of life, treatment tolerance, and survival, but cannot be prevented or reversed by current management strategies. Ursolic acid is a natural dietary compound that has been shown to inhibit atrophy-associated changes in skeletal muscle mRNA expression in rodents and dogs, leading to beneficial changes in skeletal muscle structure and function. We hypothesized that dietary supplementation with ursolic acid might help support skeletal muscle mass and function during cancer. To test this hypothesis, we investigated ursolic acid's effects in five in vivo mouse models of cancer cachexia that are driven by pancreatic, colon, and lung cancer cells of mouse and human origin. We found that dietary supplementation with ursolic acid has broad-spectrum effects toward cancer-induced skeletal muscle atrophy, significantly preserving muscle mass in all five cancer cachexia models. Ursolic acid's positive effects on muscle mass and muscle fiber size led to significant improvements in grip strength and muscle tetanic force, persisted in the presence of chemotherapy, and were not associated with discernible changes in food intake or tumor growth. Ursolic acid appeared to generate its beneficial effects in skeletal muscle by acting directly on muscle cells, inhibiting catabolic effects of tumor-derived secreted factors, and inhibiting >90% of cancer-induced changes in skeletal muscle mRNA expression. These results strongly nominate ursolic acid as a promising potential nutritional approach for supporting muscle mass and function in individuals with cancer.<b>NEW & NOTEWORTHY</b> Cancer-induced muscle wasting affects many people with cancer, reducing treatment tolerance and survival. We identified a natural dietary compound, ursolic acid, that attenuates muscle atrophy across five preclinical cancer models spanning pancreatic, colon, and lung cancer. Ursolic acid inhibits cancer-induced changes in muscle mRNA expression, preserves muscle strength, and remains protective during chemotherapy, without affecting food intake or tumor burden. These results identify ursolic acid as a promising, translatable dietary supplement for supportive cancer care.</p>","PeriodicalId":7585,"journal":{"name":"American journal of physiology. Cell physiology","volume":" ","pages":"C1800-C1811"},"PeriodicalIF":5.4,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13234760/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147873034","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":"SK channels as antiarrhythmic targets for atrial fibrillation: structural and pharmacological perspectives.","authors":"Megan K McKie, Emma H Meibom, Andreina Gil Ramirez, Luca Soattin, Bo Hjorth Bentzen","doi":"10.1152/ajpcell.00921.2025","DOIUrl":"10.1152/ajpcell.00921.2025","url":null,"abstract":"<p><p>Small-conductance Ca²⁺-activated K⁺ (SK) channels have emerged as promising atrial-selective targets for rhythm control in atrial fibrillation (AF). Genetic association studies, functional experiments, and early clinical trials collectively support a role for SK channels in atrial repolarization and AF maintenance. Recent breakthroughs in single-particle cryo-electron microscopy have provided high-resolution structures of the SK2 channel, revealing unique architectural features that underlie its low conductance and susceptibility to pharmacological modulation. Numerous studies have shown alterations in SK transcript abundance in AF in both humans and animal models. However, recent functional studies have demonstrated dynamic regulation of SK channel gating and membrane trafficking in AF, highlighting context-dependent pro- and antiarrhythmic effects. This mini review summarizes the recent structural and functional advances in our understanding of SK channels and emerging therapeutic implications for AF.</p>","PeriodicalId":7585,"journal":{"name":"American journal of physiology. Cell physiology","volume":" ","pages":"C1597-C1604"},"PeriodicalIF":5.4,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147479455","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":"Advances in cell adhesion, junction dynamics, and their pathophysiological implications.","authors":"Congying Wu","doi":"10.1152/ajpcell.00930.2025","DOIUrl":"10.1152/ajpcell.00930.2025","url":null,"abstract":"","PeriodicalId":7585,"journal":{"name":"American journal of physiology. Cell physiology","volume":" ","pages":"C1594-C1596"},"PeriodicalIF":4.7,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147687359","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}