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非奈利酮治疗糖尿病性心肌病的潜力:聚焦机制

Therapeutic potential of finerenone for diabetic cardiomyopathy: focus on the mechanisms.

作者信息

Wang Jing, Xue Haojie, He Jinyu, Deng Li, Tian Julong, Jiang Yang, Feng Jian

机构信息

Department of Cardiology, Stem Cell Immunity and Regeneration Key Laboratory of Luzhou, The Affiliated Hospital of Southwest Medical University; Southwest Medical University Affiliated Hospital Medical Group Gulin Hospital (Gulin County People's Hospital), Luzhou, Sichuan, China.

Department of Rheumatology, The Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan, China.

出版信息

Diabetol Metab Syndr. 2024 Sep 18;16(1):232. doi: 10.1186/s13098-024-01466-x.

DOI:10.1186/s13098-024-01466-x
PMID:39289758
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11409712/
Abstract

Diabetic cardiomyopathy (DCM) is a kind of myocardial disease that occurs in diabetes patients and cannot be explained by hypertensive heart disease, coronary atherosclerotic heart disease and other heart diseases. Its pathogenesis may be closely related to programmed cell death, oxidative stress, intestinal microbes and micro-RNAs. The excessive activation of mineralocorticoid receptors (MR) in DCM can cause damage to the heart and kidneys. The third-generation non-steroidal mineralocorticoid receptor antagonist (MRA), finerenone, can effectively block MR, thus playing a role in protecting the heart and kidneys. This review mainly introduces the classification of MRA, and the mechanism of action, applications and limitations of finerenone in DCM, in order to provide reference for the study of treatment plans for DCM patients.

摘要

糖尿病性心肌病(DCM)是一种发生在糖尿病患者中的心肌疾病,不能用高血压性心脏病、冠状动脉粥样硬化性心脏病等其他心脏病来解释。其发病机制可能与程序性细胞死亡、氧化应激、肠道微生物和微小RNA密切相关。DCM中盐皮质激素受体(MR)的过度激活可导致心脏和肾脏损伤。第三代非甾体类盐皮质激素受体拮抗剂(MRA)非奈利酮可有效阻断MR,从而发挥心脏和肾脏保护作用。本综述主要介绍MRA的分类,以及非奈利酮在DCM中的作用机制、应用和局限性,以便为DCM患者治疗方案的研究提供参考。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c33f/11409712/24e1f8a64f5d/13098_2024_1466_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c33f/11409712/875b68fe10a4/13098_2024_1466_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c33f/11409712/24e1f8a64f5d/13098_2024_1466_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c33f/11409712/875b68fe10a4/13098_2024_1466_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c33f/11409712/24e1f8a64f5d/13098_2024_1466_Fig2_HTML.jpg

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本文引用的文献

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Int J Mol Sci. 2024 May 5;25(9):5027. doi: 10.3390/ijms25095027.
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Research progress on morphology and mechanism of programmed cell death.程序性细胞死亡的形态学和机制研究进展。
Cell Death Dis. 2024 May 10;15(5):327. doi: 10.1038/s41419-024-06712-8.
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Phosphorylations and Acetylations of Cytochrome Control Mitochondrial Respiration, Mitochondrial Membrane Potential, Energy, ROS, and Apoptosis.
磷酸化和乙酰化细胞色素控制线粒体呼吸、线粒体膜电位、能量、ROS 和细胞凋亡。
Cells. 2024 Mar 12;13(6):493. doi: 10.3390/cells13060493.
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Gasdermin D-Mediated Pyroptosis in Diabetic Cardiomyopathy: Molecular Mechanisms and Pharmacological Implications.Gasdermin D 介导的糖尿病心肌病细胞焦亡:分子机制与药物干预。
Molecules. 2023 Nov 28;28(23):7813. doi: 10.3390/molecules28237813.
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Non-steroidal mineralocorticoid receptor antagonist finerenone ameliorates mitochondrial dysfunction via PI3K/Akt/eNOS signaling pathway in diabetic tubulopathy.非甾体类盐皮质激素受体拮抗剂非奈利酮通过 PI3K/Akt/eNOS 信号通路改善糖尿病肾小管病变中的线粒体功能障碍。
Redox Biol. 2023 Dec;68:102946. doi: 10.1016/j.redox.2023.102946. Epub 2023 Oct 24.
6
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Medicina (Kaunas). 2023 Oct 14;59(10):1830. doi: 10.3390/medicina59101830.
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The Pharmacokinetics of the Nonsteroidal Mineralocorticoid Receptor Antagonist Finerenone.非甾体类盐皮质激素受体拮抗剂费列罗酮的药代动力学。
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