Metabolism: clinical and experimental最新文献

{"title":"Non-invasive diagnosis and prognosis of MASH with fibrosis F2-F3: In need for a tailored, accessible, and affordable solution for the 21st century public health epidemic","authors":"Konstantinos Stefanakis , Jacob George , Christos S. Mantzoros","doi":"10.1016/j.metabol.2025.156296","DOIUrl":"10.1016/j.metabol.2025.156296","url":null,"abstract":"","PeriodicalId":18694,"journal":{"name":"Metabolism: clinical and experimental","volume":"169 ","pages":"Article 156296"},"PeriodicalIF":10.8,"publicationDate":"2025-05-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144012867","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Reconsidering the role of active vitamin D in preventing sarcopenia: Letter to the editor","authors":"Xinxin Luo , Juntong Liu , Li Wang","doi":"10.1016/j.metabol.2025.156274","DOIUrl":"10.1016/j.metabol.2025.156274","url":null,"abstract":"","PeriodicalId":18694,"journal":{"name":"Metabolism: clinical and experimental","volume":"170 ","pages":"Article 156274"},"PeriodicalIF":10.8,"publicationDate":"2025-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143972033","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The role of active vitamin D in preventing sarcopenia—Authors' reply","authors":"Tetsuya Kawahara , Tetsuya Inazu , Gen Suzuki","doi":"10.1016/j.metabol.2025.156293","DOIUrl":"10.1016/j.metabol.2025.156293","url":null,"abstract":"","PeriodicalId":18694,"journal":{"name":"Metabolism: clinical and experimental","volume":"170 ","pages":"Article 156293"},"PeriodicalIF":10.8,"publicationDate":"2025-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144027931","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeting RBP4–STRA6 retinol signaling disrupts adipose–prostate crosstalk: A novel strategy to suppress basal cell plasticity in androgen deprivation","authors":"Huan Xu ,&nbsp;Dajun Gao ,&nbsp;Yanting Shen ,&nbsp;Jianqing Wang ,&nbsp;Junduo Wang ,&nbsp;Jun Zhu ,&nbsp;Miao Ren ,&nbsp;Lai Wei ,&nbsp;Hailiang Hu ,&nbsp;Ming Zhan ,&nbsp;Zhong Wang ,&nbsp;Fubo Wang ,&nbsp;Bin Xu","doi":"10.1016/j.metabol.2025.156288","DOIUrl":"10.1016/j.metabol.2025.156288","url":null,"abstract":"<div><div>Metabolic rewiring is a starter for lineage plasticity, which is an important driver of prostate development, tumorigenesis and treatment resistance. Androgen-targeted therapies are central to prostate cancer (PCa) management, yet the mechanisms leading prostate development—particularly the metabolic signaling within basal cells during treatment—remain poorly understood. To fulfill this gap, we used multiple models to reveal the metabolic alterations in prostate basal cells. Our study reveals the role of the RBP4-STRA6 axis in modulating retinol metabolism and transporting retinol from adipocyte into prostate cells, contributing to prostate development and basal cell differentiation during androgen deprivation. Through multi-omics analyses, we demonstrate that RBP4-STRA6 axis dependent retinol metabolism is increased with androgen deprivation. Retinol metabolism rewiring is modulated by the androgen receptor (AR) and can regulate basal cell plasticity under androgen deprivation therapy (ADT). Retinol metabolism maintains prostate basal cell lineage plasticity during hormone therapy through the PPARγ signaling pathway, compensating for the AR signaling pathway inhibition by sustaining energy homeostasis and promoting basal cell differentiation. Notably, we identified a basal cell cluster (BC5) characterized by high Retinol metabolism and activated PPARγ signaling pathway, which plays a crucial role in basal-luminal differentiation and prostate growth. This study underscores the importance of RBP4-STRA6 dependent Retinol metabolism, mediating the crosstalk between adipocytes and prostate basal cells, in maintaining prostate development during hormone therapy and provides a foundation for future clinical interventions and diet strategies aimed at enhancing the sensitivity of androgen deprivation in prostate diseases.</div></div>","PeriodicalId":18694,"journal":{"name":"Metabolism: clinical and experimental","volume":"169 ","pages":"Article 156288"},"PeriodicalIF":10.8,"publicationDate":"2025-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143923914","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"TBC1D15 protects alcohol-induced liver injury in female mice through PLIN5-mediated mitochondrial and lipid droplet contacting","authors":"Haixia Xu ,&nbsp;Jiayu Shi ,&nbsp;Wenjun Yu ,&nbsp;Shiqun Sun ,&nbsp;Haoxiong Zhou ,&nbsp;Lu Wang ,&nbsp;Jun Ren ,&nbsp;Zhifeng Gu ,&nbsp;Qi Lu ,&nbsp;Yingmei Zhang","doi":"10.1016/j.metabol.2025.156290","DOIUrl":"10.1016/j.metabol.2025.156290","url":null,"abstract":"<div><h3>Objective</h3><div>Alcohol-induced hepatic steatosis and mitochondrial dysfunction are progressive conditions contributing to the development of alcoholic liver disease (ALD), often leading to cirrhosis and hepatocellular carcinoma. TBC1D15, a Rab7 GTPase-activating protein (GAP), has been implicated in mitochondrial homeostasis, however, its role in ALD remains elusive. This study aimed to investigate the functional role of TBC1D15 in ALD and elucidate the underlying mechanisms.</div></div><div><h3>Methods</h3><div>Female TBC1D15^flox/flox mice and hepatocyte-specific overexpression of TBC1D15 mice were fed a Lieber-DeCarli ethanol diet, which progressively increasing ethanol dosages over 8 weeks. Liver tissues were assessed using histology, transmission electron microscopy, immunofluorescence, immunoblotting, and real-time PCR techniques.</div></div><div><h3>Results</h3><div>TBC1D15 levels were markedly decreased in human ALD samples and primary hepatocytes exposed to ethanol. Hepatocyte-specific TBC1D15 overexpression attenuated alcohol-induced body weight loss, improved survival, and alleviated liver injury, lipid droplet (LD) accumulation, and hepatocyte apoptosis. TBC1D15 overexpression also protected against alcohol-induced mitochondrial dysfunction and enhanced mitochondrial fatty acid β-oxidation (FAO) by promoting interactions between mitochondria and LDs in the face of alcohol exposure. Mechanistically, TBC1D15 was translocated to mitochondrial membranes in hepatocytes in response to alcohol exposure, where it recruited PLIN5 through its 10–180 aa domain. This interaction promoted mitochondria-LD contacts and facilitated PKA-induced nuclear translocation of PLIN5. Furthermore, TBC1D15 upregulated protein levels of PPARα, PGC1α and CPT1α in hepatocytes following alcohol challenge, an effect that was nullified by PKA inhibition.</div></div><div><h3>Conclusion</h3><div>TBC1D15 plays a promising protective role in ALD injury by enhancing mitochondrial function and FAO, potentially through its interaction with PLIN5 and modulation of mitochondria-LD contacts via PKA-mediated nuclear translocation of PLIN5. These findings identify TBC1D15 as a potential therapeutic target for ALD.</div></div>","PeriodicalId":18694,"journal":{"name":"Metabolism: clinical and experimental","volume":"169 ","pages":"Article 156290"},"PeriodicalIF":10.8,"publicationDate":"2025-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144004157","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dysregulation of CRY1 impairs brain thyroid hormone pathway and promotes anxiety-like behavior in male mice","authors":"Baojiang Lv ,&nbsp;Yuanyuan Liu ,&nbsp;Yu Yang ,&nbsp;Yedi Wu ,&nbsp;Zhengxin Chen ,&nbsp;Tianpeng Zhang ,&nbsp;Fangjun Yu ,&nbsp;Yafei Shi","doi":"10.1016/j.metabol.2025.156292","DOIUrl":"10.1016/j.metabol.2025.156292","url":null,"abstract":"<div><h3>Background</h3><div>The circadian clock system plays a crucial role in influencing mood and behavior, with the clock gene <em>Cry1</em> serving as a core component of the molecular circadian clock. However, the role of CRY1 in anxiety-related behaviors and their underlying mechanisms are poorly understood.</div></div><div><h3>Methods and results</h3><div>In this study, we investigated the role of CRY1 in anxiety-related behaviors through various behavioral approaches, and assessed potential molecular alterations in key brain regions involved in behavioral responses. We found that male <em>Cry1</em>^<em>-/-</em> (<em>Cry1</em> knockout) mice developed anxiety-like behavior in both stressed and non-stressed conditions. Administration of CRY1 stabilizer KL201 significantly alleviated anxiety-like behavior in male mice. Further studies suggested involvement of the brain thyroid hormone signaling in CRY1 regulation of anxiety-like behavior, evidenced by markedly reduced brain T3 levels relation to down-regulation of OATP1C1 and DIO2 mediated by CRY1, which underlies neurogenesis deficits and contributes to anxiety. Subsequent <em>in vivo</em> and cell-based experiments confirmed that CRY1 positively regulates the expression of OATP1C1 and DIO2. Mechanistically, CRY1 regulates OATP1C1 and DIO2 through regulating the transcriptional activity of E4BP4. E4BP4 trans-inactivates OATP1C1 and DIO2 via direct binding to its specific response element in the gene promoters.</div></div><div><h3>Conclusion</h3><div>These findings underscore the critical role of CRY1 in regulating thyroid hormone and anxiety, providing insight into the underlying pathogenesis and potential treatment strategies for mood disorders.</div></div>","PeriodicalId":18694,"journal":{"name":"Metabolism: clinical and experimental","volume":"169 ","pages":"Article 156292"},"PeriodicalIF":10.8,"publicationDate":"2025-05-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143934914","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Lactylation as a metabolic epigenetic modification: Mechanistic insights and regulatory pathways from cells to organs and diseases","authors":"Cong Chen ,&nbsp;Jie Wang ,&nbsp;Xueying Zhu ,&nbsp;Shan Zhang ,&nbsp;Xiandun Yuan ,&nbsp;Jun Hu ,&nbsp;Chao Liu ,&nbsp;Lanchun Liu ,&nbsp;Zhenpeng Zhang ,&nbsp;Jun Li","doi":"10.1016/j.metabol.2025.156289","DOIUrl":"10.1016/j.metabol.2025.156289","url":null,"abstract":"<div><div>In recent years, lactylation, a novel post-translational modification, has demonstrated a unique role in bridging cellular metabolism and epigenetic regulation. This modification exerts a dual-edged effect in both cancer and non-cancer diseases by dynamically integrating the supply of metabolic substrates and the activity of modifying enzymes: on one hand, it promotes tissue homeostasis and repair through the activation of repair genes; on the other, it exacerbates pathological progression by driving malignant phenotypes. In the field of oncology, lactylation regulates key processes such as metabolic reprogramming, immune evasion, and therapeutic resistance, thereby shaping the heterogeneity of the tumor microenvironment. In non-cancerous diseases, including neurodegeneration and cardiovascular disorders, its aberrant activation can lead to mitochondrial dysfunction, fibrosis, and chronic inflammation. Existing studies have revealed a dynamic regulatory network formed by the cooperation of modifying and demodifying enzymes, and have identified mechanisms such as subcellular localization and RNA metabolism intervention that influence disease progression. Nevertheless, several challenges remain in the field. This article comprehensively summarizes the disease-specific regulatory mechanisms of lactylation, with the aim of providing a theoretical foundation for its targeted therapeutic application.</div></div>","PeriodicalId":18694,"journal":{"name":"Metabolism: clinical and experimental","volume":"169 ","pages":"Article 156289"},"PeriodicalIF":10.8,"publicationDate":"2025-05-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143948633","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Comprehensive assessment of the causal effects and metabolite mediators of glucose-lowering drug targets on cardio-renal-liver-metabolic health","authors":"Haozhang Huang ,&nbsp;Huangtao Ruan ,&nbsp;Xiaozhao Lu ,&nbsp;Shiqun Chen ,&nbsp;Jiyan Chen ,&nbsp;Ning Tan ,&nbsp;Wei Pan ,&nbsp;Jin Liu ,&nbsp;Yong Liu","doi":"10.1016/j.metabol.2025.156276","DOIUrl":"10.1016/j.metabol.2025.156276","url":null,"abstract":"<div><h3>Aims</h3><div>To investigate the relationship between glucose-lowering medications and cardio-renal-liver-metabolic (CRLM) health.</div></div><div><h3>Methods</h3><div>Two-sample Mendelian randomization (MR) was applied to assess the causal relationships between seven classes of glucose-lowering drugs and CRLM health outcomes. Genetic proxies for drug exposure were identified as cis-acting single nucleotide polymorphisms in the drug target genes, linked to both gene expression levels and glycosylated hemoglobin (HbA1c) or body mass index (BMI). Validation included colocalization and linkage disequilibrium analyses. A two-step MR strategy was employed to explore potential metabolite mediators.</div></div><div><h3>Results</h3><div>Sulfonylureas were associated with a reduced heart failure (HF) risk (odds ratio [OR] = 0.38 per standard deviation change in glucose-lowering drug target perturbation equivalent to 1 unit of HbA1c lowering, <em>P</em> = 2.46E-04) but increased aspartate aminotransferase levels (OR = 1.39, <em>P</em> = 9.50E-07). Sodium-glucose cotransporter-2 inhibitors reduced the risk of acute myocardial infarction (AMI) (OR = 0.37, <em>P</em> = 1.36E-05), venous thromboembolism (VTE) (OR = 0.48, <em>P</em> = 1.89E-04), microalbuminuria (MA) (OR = 0.49, <em>P</em> = 1.65E-06), and increased estimated glomerular filtration rate (eGFR) (OR = 1.04, <em>P</em> = 2.98E-05). They also showed a potential protective effect against general liver disorders (OR = 0.41, <em>P</em> = 4.79E-04), metabolic dysfunction-associated steatotic liver disease (MASLD) (OR = 0.25, <em>P</em> = 0.008), and metabolic syndrome (MetS) (OR = 0.63, <em>P</em> = 5.40E-04). Thiazolidinediones (TZDs) reduced the risk of AMI (OR = 0.44, <em>P</em> = 4.31E-38), hypertension (HT) (OR = 0.60, <em>P</em> = 1.40E-43), MASLD (OR = 0.53, <em>P</em> = 5.61E-05), and MetS (OR = 0.66, <em>P</em> = 1.00E-20) but increased the risk of VTE (OR = 1.40, <em>P</em> = 2.53E-07), atrial fibrillation (OR = 1.61, <em>P</em> = 1.43E-09), and alcoholic liver disease (OR = 3.00, <em>P</em> = 6.56E-11). TZDs also negatively affected eGFR (OR = 0.97, <em>P</em> = 4.68E-05) and increased blood urea nitrogen levels (OR = 1.03, <em>P</em> = 2.52E-09). Glucagon-like peptide-1 receptor agonists demonstrated significant benefits for chronic kidney disease, driven by reductions in both glucose levels (OR = 0.11, <em>P</em> = 0.016) and BMI (OR = 0.20, <em>P</em> = 0.012), with potential cardiometabolic benefits from BMI reduction. Some mediating roles of metabolites have been identified (e.g., SGLT2 inhibitors mediate effects on MA via isoleucine and TZDs mediate effects on MASLD through lipid metabolites).</div></div><div><h3>Conclusions</h3><div>Glucose-lowering medications exert significant and heterogeneous effects on CRLM health, highlighting the need for personalized treatments and further investigations into their mechanisms and long-term impacts on CRLM outcomes.</div></div>","PeriodicalId":18694,"journal":{"name":"Metabolism: clinical and experimental","volume":"169 ","pages":"Article 156276"},"PeriodicalIF":10.8,"publicationDate":"2025-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144017434","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dietary context in the association between red meat consumption and risk of type 2 diabetes","authors":"Peilu Wang ,&nbsp;Yiwen Zhang ,&nbsp;Edward L. Giovannucci","doi":"10.1016/j.metabol.2025.156277","DOIUrl":"10.1016/j.metabol.2025.156277","url":null,"abstract":"<div><h3>Background</h3><div>It has been suggested that dietary factors correlated with red meat may contribute to its adverse health effects, while consuming red meat within a healthy diet may not necessarily increase disease risk.</div></div><div><h3>Methods</h3><div>Among 204,740 participants from three prospective cohorts, we examined the association between red meat consumption and risk of type 2 diabetes (T2D) across different levels of diet quality, measured by Alternative Healthy Eating Index (AHEI)-2010 (excluding red and processed meat component), using multivariable-adjusted Cox proportional hazards models. Dietary intake was assessed using repeated food frequency questionnaires.</div></div><div><h3>Results</h3><div>During a median follow-up of 28 years, 18,868 cases were documented. Mean values were 47.3 (SD 8.5) for AHEI-2010 and 6.5 (SD 3.5), 1.8 (SD 1.5), and 4.8 (SD 2.5) servings/week for total, processed, and unprocessed red meat, respectively. Greater red meat consumption was consistently associated with a higher T2D risk across AHEI-2010 strata. Comparing the highest with the lowest quintile of red meat consumption in the highest diet quality quintile, the multivariable-adjusted HRs were 1.95 (1.72, 2.21) for total, 1.88 (1.67, 2.13) for processed, and 1.67 (1.47, 1.90) for unprocessed red meat. Substituting red meat with major food groups was associated with a lower T2D risk, particularly among those with high diet quality. The benefit of lowering red meat consumption was greater in participants with higher diet quality.</div></div><div><h3>Conclusions</h3><div>The risk associated with high red meat consumption persisted even among participants with a relatively high diet quality, underscoring the importance of limiting red meat consumption to prevent T2D.</div></div>","PeriodicalId":18694,"journal":{"name":"Metabolism: clinical and experimental","volume":"169 ","pages":"Article 156277"},"PeriodicalIF":10.8,"publicationDate":"2025-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143918469","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Angiotensinogen inhibition concurrently mitigates alcohol-associated hepatic and muscle injury","authors":"Zhaodi Che ,&nbsp;Mingxiang Cai ,&nbsp;Xiaowu Dong ,&nbsp;Yuan Yuan ,&nbsp;Yaodong Wang ,&nbsp;Lu Xiao ,&nbsp;Yali Song ,&nbsp;Jiajun Zhong ,&nbsp;Pingping Luo ,&nbsp;Hao Wang ,&nbsp;Guotao Lu ,&nbsp;Yao Sun ,&nbsp;Jia Xiao","doi":"10.1016/j.metabol.2025.156275","DOIUrl":"10.1016/j.metabol.2025.156275","url":null,"abstract":"<div><h3>Aims</h3><div>The organ communication mechanisms driven by alcohol-associated liver disease (ALD) remain inadequately understood. This study explores the endocrine roles of the hepatokine angiotensinogen (AGT) and the renin-angiotensin system (RAS) in ALD.</div></div><div><h3>Methods and results</h3><div>Hepatokine screening tests revealed that chronic-binge ethanol consumption upregulates hepatic AGT production, triggering downstream RAS activation. Hepatocyte-specific knockout of <em>Agt</em> (AGT^ΔHep) significantly alleviated ALD-induced liver injury. In organ screening between AGT^flox/flox (AGT^f/f) and AGT^ΔHep mice, skeletal muscle exhibited the most pronounced improvement in alcoholic myopathy (AM)-related phenotypes, including reduced muscle mass, enhanced oxidative stress, and mitochondrial dysfunction post-ethanol administration. Mechanistically, the renin-angiotensin axis transmits damaging signals from AGT to their membrane receptor AGTR1 in both hepatocytes and myocytes. Pharmacological inhibition of AGT, renin, and angiotensin-converting enzyme, as well as specific knockdown of <em>Agtr1</em> in hepatocytes or myocytes, effectively attenuated both conditions. Activation of the counteractive axis of the RAS-AGTR1 pathway, involving Ang (1–7) and its membrane receptor MAS1, ameliorated the alcoholic injury of both the liver and muscle. Conversely, specific knockdown of <em>Mas1</em> in hepatocytes and myocytes exacerbated these injuries.</div></div><div><h3>Conclusions</h3><div>Our work demonstrates that hepatokine AGT promotes ALD and AM through the activation of the RAS-AGTR1 axis and the inhibition of the Ang(1–7)-MAS1 axis, offering a foundation for concurrent therapeutic strategies for both diseases.</div></div>","PeriodicalId":18694,"journal":{"name":"Metabolism: clinical and experimental","volume":"169 ","pages":"Article 156275"},"PeriodicalIF":10.8,"publicationDate":"2025-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143918468","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}