American journal of physiology. Cell physiology最新文献

{"title":"Sex-specific dysregulation of cardiac-enriched microRNAs with age in <i>Drosophila melanogaster</i>.","authors":"Lijo N Varghese, Philip W Sheard, Daryl O Schwenke, Rajesh Katare","doi":"10.1152/ajpcell.00134.2025","DOIUrl":"10.1152/ajpcell.00134.2025","url":null,"abstract":"<p><p>Dysregulation of cardiac-enriched microRNA (miRNA) expression is linked to age-associated cardiovascular diseases (CVDs). However, the sex-specificity and age at which dysregulation occurs remain unclear. Given the conserved nature of miRNAs and short lifespan of <i>Drosophila melanogaster</i> (fruit flies), we investigated age-related changes in the expression of cardiac enriched miRNAs (miR-1, -9, -34a, and -133, target miRNAs) and their impact on the cardiac tube in male and female flies. Cardiac tube tissues were collected from male and female flies (<i>n</i> = 5/group) at 7-day intervals from <i>day 7</i> to <i>day 70</i>. miRNAs and predicted target mRNA gene (<i>KCNQ</i>, <i>MRTF</i>, and <i>CCN</i>) expression were quantified by RT-qPCR (<i>n</i> = 4-6/group). Myofibril diameter was assessed by Masson's trichrome staining (<i>n</i> = 4-6) to determine the structural effects of hypertrophic miR-9. In females, miR-1 was downregulated with age (<i>P</i> ≤ 0.0001), whereas in males, miR-9 (<i>P</i> ≤ 0.0001) and miR-34a (<i>P</i> = 0.0017) were downregulated. Interestingly, miR-133 was downregulated in both sexes (<i>P</i> ≤ 0.0001). In males, <i>MRTF</i> (miR-9 target) and <i>CCN</i> (miR-133 target) expression increased with age (<i>P</i> = 0.016 and <i>P</i> = 0.013, respectively), whereas in females, <i>KCNQ</i> (miR-1 target) and <i>CCN</i> expression decreased (<i>P</i> = 0.03 and <i>P</i> = 0.002, respectively). Myofibril thickness significantly increased with age in both sexes (<i>P</i> < 0.0001). miR-9 downregulation may contribute to this effect in males, whereas the mechanism in females remains unclear. This study provides novel insights into sex-specific miRNA dysregulation in cardiac aging, emphasizing the need to consider sex differences in miRNA-mediated cardiovascular aging and the potential of miRNAs as diagnostic tools in age-related CVDs.<b>NEW & NOTEWORTHY</b> Advancements in healthcare and diet have increased life expectancy, doubling the population aged 60 and above by 2050. However, this longevity raises the risk of chronic diseases, especially cardiovascular diseases. We examined age-related changes in cardiovascular-enriched microRNAs in the <i>Drosophila melanogaster</i> heart. This first-of-its-kind observational study tracks microRNA changes across life stages. It highlights sex-specific expression of miRNAs, providing crucial insights into cardiac aging. It lays a strong foundation for future research on microRNA in heart health.</p>","PeriodicalId":7585,"journal":{"name":"American journal of physiology. Cell physiology","volume":" ","pages":"C1743-C1751"},"PeriodicalIF":5.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143958271","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":"GLP-1 and ghrelin inversely regulate insulin secretion and action in pancreatic islets, vagal afferents, and hypothalamus for controlling glycemia and feeding.","authors":"Toshihiko Yada, Katsuya Dezaki, Yusaku Iwasaki","doi":"10.1152/ajpcell.00168.2025","DOIUrl":"https://doi.org/10.1152/ajpcell.00168.2025","url":null,"abstract":"<p><p>Glucagon-like peptide-1 (GLP-1) was discovered as an incretin hormone, which is released from the intestine upon nutrient intake and stimulates insulin secretion from the pancreatic islet β-cells. Subsequently, its ability to suppress appetite was recognized. Ghrelin, discovered as the ligand for growth hormone secretagogue-receptor (GHS-R), is released from the stomach and produces appetite. Later, its ability to inhibit insulin secretion and elevate blood glucose was found. Thus, GLP-1 and ghrelin regulate insulin secretion and appetite toward opposite directions. The receptor agonists for GLP-1 and ghrelin have been developed and are now used to treat metabolic diseases, in which insulin plays a key role. However, underlying action mechanism and possible interplay of these hormones have remained elusive. Here, we describe that GLP-1 and ghrelin reciprocally regulate the insulin system. GLP-1 enhances and ghrelin suppresses insulin secretion in pancreatic β-cells. Moreover, GLP-1 cooperates with and ghrelin counteracts insulin action in the vagal afferent and hypothalamic arcuate nucleus (ARC) neurons, the interfaces between the peripheral metabolism and brain. Notably, ghrelin rises and works preprandially and GLP-1 rises and works postprandially. The interplay of ghrelin, GLP-1, and insulin leads to optimal circadian control of feeding, glycemia, and metabolism.</p>","PeriodicalId":7585,"journal":{"name":"American journal of physiology. Cell physiology","volume":"328 6","pages":"C1793-C1807"},"PeriodicalIF":5.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143964789","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":"Immunoproteasome subunit PSMB8 promotes skeletal muscle regeneration by regulating macrophage phenotyping switch in mice.","authors":"Yanhong Zhang, Shiyao Hong, Fan Zhang, Kexin Yao, Shuhui Jin, Shijuan Gao, Yan Liu, Yulin Li, Congcong Zhang","doi":"10.1152/ajpcell.00965.2024","DOIUrl":"https://doi.org/10.1152/ajpcell.00965.2024","url":null,"abstract":"<p><p>Immunoproteasomes regulate the degradation of ubiquitin-coupled proteins and cell differentiation. However, its precise role in skeletal muscle regeneration remains unclear. In this study, we found that expression of the immunoproteasome subunit, PSMB8, increased significantly in young muscles after cardiotoxin-induced injury, whereas its expression was downregulated in injured aged mice. Genetic knockout or pharmacological inhibition of the immunoproteasome subunit, PSMB8, resulted in impaired muscle regeneration and increased interstitial fibrosis. PSMB8 inhibition by short interfering RNA (siRNA) or inhibitor decreased the differentiation ability of myoblasts. There was increased infiltration of inflammatory cells, especially Ly6C^hi proinflammatory macrophages, in <i>Psmb8</i> deficient muscles. In vitro, <i>Psmb8-</i>deficient macrophages expressed higher levels of proinflammatory cytokines and lower levels of anti-inflammatory cytokines after phagocytosis of myoblast debris, which was associated with increased activation of the NF-κB signaling pathway. Inhibition of the NF-κB pathway improves the regeneration ability and attenuates interstitial fibrosis in <i>Psmb8-</i>deficient muscles after injury. The overexpression of <i>Psmb8</i> by adenovirus could also improve the regenerative ability of aged muscles.<b>NEW & NOTEWORTHY</b> The immunoproteasome subunit, PSMB8, is essential for efficient muscle regeneration and may be a new therapeutic target for age-related muscle atrophy.</p>","PeriodicalId":7585,"journal":{"name":"American journal of physiology. Cell physiology","volume":"328 6","pages":"C1716-C1729"},"PeriodicalIF":5.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143952251","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":"Biomechanical platelet activation: diseases that require a new class of antiplatelet therapeutics.","authors":"Riya Gupta, Fahad Alkhalfan, Jason Wheeler, Scott J Cameron","doi":"10.1152/ajpcell.00228.2025","DOIUrl":"10.1152/ajpcell.00228.2025","url":null,"abstract":"<p><p>Mechanisms of platelet activation have traditionally been investigated through the activation of biochemical pathways through cell surface agonists such as adenosine diphosphate, thrombin, and collagen. However, recent research has identified another crucial mechanism, biomechanical activation, where external physical forces directly influence platelet reactivity. This paradigm shift underscores the complex interplay between biochemical and biomechanical stimuli in platelet activation. This review aims to understand the molecular mechanisms underlying biomechanical activation and the implications for treating thrombotic disorders.</p>","PeriodicalId":7585,"journal":{"name":"American journal of physiology. Cell physiology","volume":" ","pages":"C1831-C1836"},"PeriodicalIF":5.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143953459","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":"Macrophage heme oxygenase-1 modulates peroxynitrite-mediated vascular injury and exacerbates abdominal aortic aneurysm development.","authors":"Liangliang Jia, Yufei Wang, Chunna Jin, Yuankun Ma, Yidong Wang, Liuguang Song, Jian Shen, Yao Xie, Meixiang Xiang","doi":"10.1152/ajpcell.00525.2023","DOIUrl":"https://doi.org/10.1152/ajpcell.00525.2023","url":null,"abstract":"<p><p>Inflammatory reactions mediated by macrophages are profoundly related to the depletion of smooth muscle cells (SMCs) in abdominal aortic aneurysm (AAA) development. The findings from our previous investigation indicate that heme oxygenase-1 (HO-1) in macrophages exacerbates proinflammatory responses and oxidative damage. Therefore, the aim of this work was to gain insight into the function of HO-1 derived from macrophages and elucidate the underlying molecular mechanisms involved in AAA development. In this study, we discovered a dramatic increase in HO-1 expression in the infiltrated macrophages in experimental calcium phosphate-induced AAA tissues. Myeloid conditional HO-1-deficient mice displayed slower luminal area enlargement, as well as diminished inducible nitric oxide synthase (iNOS)-positive M1 macrophage activation, peroxynitrite generation, and SMCs apoptosis in aneurysmal tissues compared with littermate controls. Furthermore, we showed that inhibiting HO-1 eliminated the protein expression of iNOS induced by lipopolysaccharide/interferon-γ in bone marrow-derived macrophages, whereas the mRNA expression remained unaffected. Suppressing iNOS in macrophages alleviated SMCs apoptosis by decreasing nitric oxide generation in a coculture system in vitro. In summary, our study illustrates that macrophage-derived HO-1 strengthens AAA development through boosting the production of iNOS-dependent peroxynitrite and the deterioration of SMCs. These findings reveal potential therapeutic targets for resolving aneurysmal diseases.<b>NEW & NOTEWORTHY</b> This article illustrates the role of macrophage-derived heme oxygenase-1 (HO-1) in the development of abdominal aortic aneurysm (AAA). HO-1 deletion in macrophages hindered AAA development by reducing inducible nitric oxide synthase (iNOS)-dependent peroxynitrite production and smooth muscle cells (SMCs) apoptosis in vivo. Mechanistically, inhibition of HO-1 reduced the stimulated iNOS protein production in macrophages by lipopolysaccharide/interferon-γ. Moreover, suppressing iNOS in macrophages prevented SMCs apoptosis by decreasing nitric oxide generation in vitro.</p>","PeriodicalId":7585,"journal":{"name":"American journal of physiology. Cell physiology","volume":"328 6","pages":"C1808-C1821"},"PeriodicalIF":5.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143965948","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":"GLP-1 receptor agonists in the context of cancer: the road ahead.","authors":"Isabelle R Miousse","doi":"10.1152/ajpcell.00245.2025","DOIUrl":"10.1152/ajpcell.00245.2025","url":null,"abstract":"<p><p>A rapidly increasing proportion of the population in the United States is taking glucagon-like peptide-1 receptor agonists (GLP-1RAs) for type 2 diabetes or weight loss. Consequently, an increasing number of patients presenting with new cases of cancer also have a current prescription for GLP-1RAs. The impact of GLP-1RAs on metabolism is quite profound, and it is entirely reasonable to assume these agents are also very impactful on the metabolism of cancer cells, in addition to the general metabolism of the patient. Although these drugs are relatively recent on the market, the study of metabolism in cancer is a well-established field and we can make predictions about how GLP-1RAs will interface with cancer treatments. In fact, some evidence points to a possible neoadjuvant effect of these drugs for patients with cancer that would justify the initiation of GLP-1RAs to support therapy in a subset of patients. At the same time, there is a very present concern that drugs that induce weight loss may also precipitate the loss of muscle mass, cachexia, in patients. Here, we will provide an overview of the existing literature around diabetes and metabolism in the context of cancer and cachexia.</p>","PeriodicalId":7585,"journal":{"name":"American journal of physiology. Cell physiology","volume":" ","pages":"C1822-C1828"},"PeriodicalIF":5.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143959390","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":"AAV1-CFTR preferentially transduces cysts and reduces cyst size in a mouse model of ADPKD.","authors":"Cristian Ciobanu, Liudmila Cebotaru","doi":"10.1152/ajpcell.00057.2025","DOIUrl":"https://doi.org/10.1152/ajpcell.00057.2025","url":null,"abstract":"<p><p>To overcome the challenges of developing a gene therapy for autosomal dominant polycystic kidney disease (ADPKD), we focused on the surface receptors expressed in cystic epithelia. Importantly, we detected altered localization in the cystic epithelium of wheat germ agglutinin, WGA, staining of sialic acids. Throughout the membrane of the cysts, we saw altered staining with <i>Maackia amurensis</i> lectin (MAL) or with <i>Sambucus nigra</i> lectin (SNL) that are specific for α2,3- and α2,6-<i>N</i>-linked sialic acids, respectively. Given that these sialic acid glycoproteins facilitate the transduction of adeno-associated virus 1 (AAV1), we injected 1-mo-old, <i>pkd1^{R3277C/R3277C}</i>, (RC/RC) ADPKD mice intraperitoneally with 2 × 10¹² particles/kg of AAV1 containing either a green fluorescent protein (GFP) vector or a truncated cystic fibrosis transmembrane conductance regulator (CFTR) vector, Δ27-264-CFTR. Two months after treatment, the cyst area and size were significantly lower in the CFTR vector-treated mice compared with those untreated and those receiving the GFP. We detected vector genomes and mRNA expression only in their corresponding CFTR vector- or GFP vector-treated mice. We observed co-staining for GFP and CFTR immunofluorescence with either the Na⁺/H⁺ exchanger or epithelial Na⁺ channel, indicating proximal tubule or collecting duct expression, respectively. Expression of GFP and CFTR protein expression above background levels was detected. CFTR immunofluorescence was increased in the basolateral membrane after CFTR vector instillation. Finally, these data suggest that cysts are prime targets for AAV1 gene therapy and offer an exciting prospect for ADPKD gene therapy.<b>NEW & NOTEWORTHY</b> Current therapies for ADPKD involve treatment of the symptoms. A direct approach would involve a gene therapy. Here we show AAV1 is tropic for cystic epithelia, which have abundant expression of sialic acid resides known to enhance AAV1 transduction. We show that a CFTR-based vector can reduce cyst size, suggesting that it may be therapeutic. These data suggest that cysts are prime targets for AAV1 and offer an exciting prospect for ADPKD gene therapy.</p>","PeriodicalId":7585,"journal":{"name":"American journal of physiology. Cell physiology","volume":"328 6","pages":"C1783-C1792"},"PeriodicalIF":5.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143963791","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":"Decorin the antifibrotic proteoglycan and its progression in therapy.","authors":"Kornélia Baghy, Helga Szakadáti, Ilona Kovalszky","doi":"10.1152/ajpcell.01075.2024","DOIUrl":"10.1152/ajpcell.01075.2024","url":null,"abstract":"<p><p>Fibrosis, which underlies numerous chronic diseases, is characterized by excessive extracellular matrix (ECM) accumulation, resulting in disrupted tissue architecture. Decorin, a small leucine-rich proteoglycan synthesized primarily by fibroblasts and myoblasts, has emerged as a potent antifibrotic agent mainly by inhibiting transforming growth factor-β (TGF-β), which is a major driver of fibrosis in various tissues and organs such as the heart, eyes, skin, liver, muscle, etc. Numerous therapeutic applications of decorin showcase its ability to reduce fibrosis and improve tissue function. Advances in treatments utilizing recombinant protein, gene-delivery systems, and biomaterials, such as decorin-loaded hydrogels, have demonstrated decorin's potential to improve localized and systemic fibrosis therapies. This review discusses recent advances in decorin's antifibrotic potential and its therapeutic applications.</p>","PeriodicalId":7585,"journal":{"name":"American journal of physiology. Cell physiology","volume":" ","pages":"C1853-C1865"},"PeriodicalIF":5.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143966197","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":"Interleukin-6 from the adipose secretome potentiate differentiation of adipose progenitors through the activation of redox signaling.","authors":"Jessica L Wager, Larissa G Baker, Taylor B Scheidl, Sophie Z Yonan, Pina Colarusso, Daniel Young, Antoine Dufour, Jennifer A Thompson","doi":"10.1152/ajpcell.00024.2025","DOIUrl":"https://doi.org/10.1152/ajpcell.00024.2025","url":null,"abstract":"<p><p>Under obesogenic conditions, it is thought that a signal arising from the adipose microenvironment triggers differentiation of adipose progenitor cells (APCs); yet the identity and source of this signal remain unknown. Redox signaling was shown to influence adipogenesis in primary murine APCs treated with pharmacological agents to manipulate the levels of reactive oxygen species (ROS). Increased generation of superoxide ([Formula: see text]) and hydrogen peroxide (H₂O₂) via redox cyclers amplified APC differentiation, while differentiation was blunted with ROS scavengers and antioxidants. Protein was concentrated from conditioned media of adipose tissue explants cultured ex vivo to capture secreted factors. Differentiation was enhanced in APCs cultured in the presence of the adipose protein secretome, an effect that was diminished with scavenging of ROS and amplified when the secretome was collected from mice fed a high-fat diet. Proteomic analysis revealed that the adipose secretome from animals on a high-fat diet was enriched in pathways involved in immune cell responses and contained higher levels of cytokines, including interleukin 6 (IL-6). A multiplex assay confirmed higher IL-6, which was predicted as a central regulator of differential levels of secretome proteins. Exposure of APCs to IL-6 increased adipogenesis, while treatment of APCs with an IL-6 blocking antibody diminished the adipogenic effect of the adipose secretome. Together, these findings substantiate a role for redox signaling in the regulation of adipogenesis and identify IL-6 as a potential secreted factor that may mediate activation of adipogenesis via ROS generation under obesogenic conditions.<b>NEW & NOTEWORTHY</b> This study identified IL-6 as an adipose-secreted factor that is increased in obesity and potentiates differentiation of APCs. Redox signaling is involved in APC differentiation and mediates the proadipogenic effect of IL-6. Thus, IL-6 may be a paracrine regulator of APC differentiation in the setting of obesity.</p>","PeriodicalId":7585,"journal":{"name":"American journal of physiology. Cell physiology","volume":"328 6","pages":"C1730-C1742"},"PeriodicalIF":5.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143962568","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":"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}