[线粒体动力学在糖尿病心肌病中的作用及调控机制]。

Q3 Medicine
生理学报 Pub Date : 2024-02-25
Huan Yue, De-Ma De, Ming-Ge Ding, Feng Fu
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引用次数: 0

摘要

心血管并发症是糖尿病患者死亡的主要原因。其中,糖尿病心肌病(DCM)是一种特殊的心肌病,不包括高血压和冠心病引起的心肌损害。其特点是心肌细胞代谢异常和心脏功能逐渐衰退。DCM 的临床表现为早期舒张功能受损,晚期收缩功能受损。最终发展为心力衰竭。线粒体是心肌细胞中提供能量的主要细胞器。线粒体动力学是指线粒体融合和分裂的动态过程,是线粒体质量控制的重要方法。线粒体动力学在维持线粒体平衡和心脏功能方面起着至关重要的作用。调控线粒体裂变的蛋白质主要是 Drp1 及其受体、Fis1、MFF、MiD49 和 MiD51。执行线粒体外膜融合的蛋白是 Mfn1/2,内膜融合蛋白是 Opa1。本文回顾了 DCM 线粒体动力学的最新进展。主要内容如下:1 型和 2 型 DCM 的线粒体动力学失衡均表现为裂变增加和融合抑制。前者的分子机制主要与 Drp1 上调和 Opa1 下调有关,后者的分子机制主要与 Drp1 上调和 Mfn1/2 下调有关。线粒体裂变增加和融合抑制可导致线粒体功能障碍,促进 DCM 的发展。中药中的有效成分,如番泻叶苷、芍药酚和内源性物质褪黑素,可通过抑制线粒体裂变或促进线粒体融合,改善线粒体功能,缓解 DCM 的症状。本文有助于进一步了解线粒体动力学在DCM中的作用和机制,为临床DCM患者提供基于线粒体动力学的新的治疗方法和干预策略。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
[Role of mitochondrial dynamics in diabetic cardiomyopathy and regulatory mechanisms].

Cardiovascular complications are the leading cause of death in diabetic patients. Among them, diabetic cardiomyopathy (DCM) is a type of specific cardiomyopathy excluding myocardial damage caused by hypertension and coronary heart disease. It is characterized by abnormal metabolism of cardiomyocytes and gradual decline of cardiac function. The clinical manifestations of DCM are impaired diastolic function in early stage and impaired systolic function in late stage. Eventually it developed into heart failure. Mitochondria are the main organelles that provide energy in cardiomyocytes. Mitochondrial dynamics refers to the dynamic process of mitochondrial fusion and fission, which is an important approach for mitochondrial quality control. Mitochondrial dynamics plays a crucial role in maintaining mitochondrial homeostasis and cardiac function. The proteins that regulate mitochondrial fission are mainly Drp1 and its receptors, Fis1, MFF, MiD49 and MiD51. The protein that performs mitochondrial outer membrane fusion is Mfn1/2, and the inner membrane fusion protein is Opa1. This paper reviews recent progress on mitochondrial dynamics in DCM. The main contents are as follows: mitochondrial dynamics imbalance in both type 1 and 2 DCM is manifested as increased fission and inhibited fusion. The molecular mechanism of the former is mainly associated with up-regulated Drp1 and down-regulated Opa1, while the molecular mechanism of the latter is mainly associated with up-regulated Drp1 and down-regulated Mfn1/2. Increased mitochondrial fission and inhibited fusion can lead to mitochondrial dysfunction and promote the development of DCM. The active ingredients of the traditional Chinese medicine such as punicalagin, paeonol and endogenous substance melatonin can improve mitochondrial function and alleviate the symptoms of DCM by inhibiting mitochondrial fission or promoting mitochondrial fusion. This article is helpful to further understand the role and mechanism of mitochondrial dynamics in DCM, and provide new treatment methods and intervention strategies for clinical DCM patients based on mitochondrial dynamics.

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来源期刊
生理学报
生理学报 Medicine-Medicine (all)
CiteScore
1.20
自引率
0.00%
发文量
4820
期刊介绍: Acta Physiologica Sinica (APS) is sponsored by the Chinese Association for Physiological Sciences and Shanghai Institutes of Biological Sciences, Chinese Academy of Sciences (CAS), and is published bimonthly by the Science Press, China. APS publishes original research articles in the field of physiology as well as research contributions from other biomedical disciplines and proceedings of conferences and symposia of physiological sciences. Besides “Original Research Articles”, the journal also provides columns as “Brief Review”, “Rapid Communication”, “Experimental Technique”, and “Letter to the Editor”. Articles are published in either Chinese or English according to authors’ submission.
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