The Role of Mitochondrial Dysfunction and Dynamics in Hypertensive Heart Disease: Mechanisms and Recent Advances.

IF 3.5 3区 生物学 Q1 BIOLOGY
Bislom C Mweene, Hanzooma Hatwiko, Joreen P Povia, Sepiso K Masenga
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Abstract

Hypertensive heart disease (HHD) is characterized by pressure overload-induced cardiac remodeling, in which mitochondrial dysfunction has emerged as a central contributor to pathophysiology. Mitochondria occupy roughly one-third of the volume of a cardiomyocyte and serve as the primary source of ATP for the constantly active heart, while also regulating calcium homeostasis, redox balance, and apoptotic signaling. Chronic hypertension imposes energetic and oxidative stress on cardiomyocytes, disrupting mitochondrial structure and function. Key mitochondrial quality control processes including organelle fusion-fission dynamics, biogenesis, and mitophagy become dysregulated in HHD, leading to impaired energy production and heightened cell injury. This unstructured review discusses the physiological roles of mitochondria in cardiac muscle and examines how altered mitochondrial dynamics contribute to hypertensive cardiac damage. We detail mechanisms of mitochondrial dysfunction in HHD, such as excessive fission, cristae disruption, and oxidative stress, and how these changes are exacerbated by aging. Age-related mitochondrial remodeling such as loss of cristae and decreased organelle volume may synergistically worsen hypertensive cardiac injury. We further integrate findings from recent studies in animal and human models, including advanced three-dimensional ultrastructural analyses and molecular investigations that illuminate new aspects of mitochondrial network organization, the mitochondrial contact site and cristae organizing system (MICOS), cristae maintenance complex, and quality control pathways in HHD. Understanding mitochondrial dysfunction in HHD reveals potential therapeutic avenues targeting mitochondrial quality and dynamics to preserve cardiac function in hypertension.

线粒体功能障碍和动力学在高血压心脏病中的作用:机制和最新进展。
高血压心脏病(HHD)的特征是压力过载引起的心脏重构,其中线粒体功能障碍已成为病理生理学的核心因素。线粒体约占心肌细胞体积的三分之一,是持续活跃的心脏ATP的主要来源,同时也调节钙稳态、氧化还原平衡和凋亡信号。慢性高血压对心肌细胞施加能量和氧化应激,破坏线粒体结构和功能。关键的线粒体质量控制过程,包括细胞器融合裂变动力学、生物发生和线粒体自噬在HHD中变得失调,导致能量产生受损和细胞损伤加剧。这篇非结构化的综述讨论了线粒体在心肌中的生理作用,并探讨了线粒体动力学的改变如何导致高血压心脏损伤。我们详细介绍了HHD线粒体功能障碍的机制,如过度裂变、嵴破坏和氧化应激,以及这些变化如何随着年龄的增长而加剧。年龄相关的线粒体重塑,如嵴的丧失和细胞器体积的减少可能协同加重高血压心脏损伤。我们进一步整合了动物和人类模型的最新研究成果,包括先进的三维超微结构分析和分子研究,阐明了线粒体网络组织、线粒体接触点和嵴组织系统(MICOS)、嵴维持复合体和HHD质量控制途径的新方面。了解HHD的线粒体功能障碍揭示了针对线粒体质量和动力学的潜在治疗途径,以保护高血压患者的心功能。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Biology-Basel
Biology-Basel Biological Science-Biological Science
CiteScore
5.70
自引率
4.80%
发文量
1618
审稿时长
11 weeks
期刊介绍: Biology (ISSN 2079-7737) is an international, peer-reviewed, quick-refereeing open access journal of Biological Science published by MDPI online. It publishes reviews, research papers and communications in all areas of biology and at the interface of related disciplines. Our aim is to encourage scientists to publish their experimental and theoretical results in as much detail as possible. There is no restriction on the length of the papers. The full experimental details must be provided so that the results can be reproduced. Electronic files regarding the full details of the experimental procedure, if unable to be published in a normal way, can be deposited as supplementary material.
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