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醛固酮和盐皮质激素受体在代谢功能障碍相关脂肪性肝病中的作用

The Role of Aldosterone and the Mineralocorticoid Receptor in Metabolic Dysfunction-Associated Steatotic Liver Disease.

作者信息

Barigou Mohammed, Ramzan Imran, Chartoumpekis Dionysios V

机构信息

Department of Diabetes, College of Health Sciences, University of Doha for Science and Technology, Doha 24449, Qatar.

Division of Endocrinology, School of Medicine, University of Patras, 26500 Patras, Greece.

出版信息

Biomedicines. 2025 Jul 22;13(8):1792. doi: 10.3390/biomedicines13081792.

DOI:10.3390/biomedicines13081792
PMID:40868048
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12383379/
Abstract

Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD) is one of the fastest-growing hepatic disorders worldwide. During its natural course, MASLD tends to progress from isolated steatosis of the liver to Metabolic Dysfunction-Associated Alcoholic Steatohepatitis (MASH), advanced fibrosis, and finally cirrhosis, with the risk of developing hepatocellular carcinoma (HCC). Although frequently related to overweight or obesity and other components of the metabolic syndrome (MS), MASLD can also be present in individuals without such risk factors. The mechanisms leading to MASLD are incompletely elucidated and may involve many proinflammatory and pro-fibrotic pathways, disrupted biliary acid homeostasis, and gut microbiota dysbiosis. Aldosterone and its interaction with the mineralocorticoid receptor (MR) are thought to participate in the pathogenesis of MASLD through the modulation of inflammation and fibrosis. Remarkably, blockade of the MR in experimental models was shown to improve MASH and fibrosis through mechanisms that need further characterization. So far, however, few clinical studies have explored the effect of MR blockade in the management of MASH and associated fibrosis. This review is intended to summarize the recent animal and human data concerning the interaction between MR pathways and MASLD.

摘要

代谢功能障碍相关脂肪性肝病(MASLD)是全球范围内增长最快的肝脏疾病之一。在其自然病程中,MASLD往往从单纯性肝脂肪变性发展为代谢功能障碍相关酒精性脂肪性肝炎(MASH)、进展性肝纤维化,最终发展为肝硬化,并伴有肝细胞癌(HCC)的发生风险。尽管MASLD常与超重、肥胖及代谢综合征(MS)的其他组分相关,但无此类危险因素的个体也可能发生MASLD。导致MASLD的机制尚未完全阐明,可能涉及许多促炎和促纤维化途径、胆汁酸稳态破坏以及肠道微生物群失调。醛固酮及其与盐皮质激素受体(MR)的相互作用被认为通过调节炎症和纤维化参与MASLD的发病机制。值得注意的是,在实验模型中,MR阻断可通过尚需进一步明确的机制改善MASH和肝纤维化。然而,迄今为止,很少有临床研究探讨MR阻断在MASH及相关肝纤维化治疗中的作用。本综述旨在总结近期有关MR通路与MASLD相互作用的动物和人体研究数据。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/258f/12383379/8b63e3eaccee/biomedicines-13-01792-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/258f/12383379/f0cd1fa3dcee/biomedicines-13-01792-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/258f/12383379/8b63e3eaccee/biomedicines-13-01792-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/258f/12383379/f0cd1fa3dcee/biomedicines-13-01792-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/258f/12383379/8b63e3eaccee/biomedicines-13-01792-g002.jpg

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