Mechanistic insight of mitochondrial dysfunctions in cardiovascular diseases with potential biomarkers

IF 1.1 4区 医学 Q4 TOXICOLOGY
Md. Nazmul Islam, Vineet Kumar Mishra, Rina Munalisa, Farzana Parveen, Saieeda Fabia Ali, Khadiza Akter, Tanvir Ahmed, Tsung-Jung Ho, Chih-Yang Huang
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引用次数: 0

Abstract

Background

Acceleration of atherogenesis is an aftermath of cardiovascular diseases (CVDs), which arise with mitochondrial dysfunction (MD). Endothelium restraint inflammation, repair and fluidic exchange with nearby tissues. Endothelium-mediated mitochondrial damage can trigger the molecular mechanisms of vasodilation, pro-inflammation and process of pro-thrombotic accumulation in microvascular endothelial layer. The oxidation of lipid particles generates modified lipoproteins. Modification of mitochondrial function recently emerged a great concern towards the atherosclerosis initiation and progression, because the powerhouse of energy production mitochondria mutation can release mtDNA into cytoplasm and it can be act as sensor for viral DNA or foreign DNA. Another cause is mitochondrial imbalance can lead to product excess amount of reactive oxygen species (ROS) which can cause cellular metabolism and respiration system.

Objectives

In previous some studies showed that mitochondrial dysfunction plays a vital role in term of cardiac diseases. However, very few studies provide evidence of endothelium-mediated mitochondrial imbalance. This study investigated the potential involvement of mitochondrial impairment in cardiotoxicity using a series of mechanistic endpoints, including mitochondrial respiration and endothelial suppression of inflammation, mitochondrial DNA. Our study provides some molecular mechanisms regarding mitochondrial role in endothelium function. In each section, we are trying to introduce key concepts and then analysis previous studies revealed the importance of that molecular mechanism regarding mitochondrial dysfunction.

Conclusions

The ultimate goal of our review is to find out the novel drug discovery or new approaches of therapy. Our review will target different aspects of mitochondrial protein function and their effect of endothelial and cause of atherosclerosis diseases. To evaluate the healthy lifestyle and better condition of mitochondrial balance nowadays it is urgent to utilize the proper function for therapeutical effect for future direction.

Abstract Image

线粒体功能障碍在心血管疾病中的机理研究及潜在生物标志物
背景加速动脉粥样硬化是心血管疾病(CVDs)的后遗症,而心血管疾病的发生与线粒体功能障碍(MD)有关。内皮抑制炎症、修复和与附近组织的液体交换。内皮介导的线粒体损伤可触发微血管内皮层的血管扩张、促炎症和促血栓形成过程的分子机制。脂质颗粒的氧化会产生改性脂蛋白。线粒体功能的改变最近引起了人们对动脉粥样硬化发生和发展的极大关注,因为产生能量的动力源线粒体发生突变会将 mtDNA 释放到细胞质中,从而成为病毒 DNA 或外来 DNA 的感应器。另一个原因是线粒体失衡会导致产生过量的活性氧(ROS),从而引起细胞代谢和呼吸系统紊乱。然而,很少有研究提供内皮介导的线粒体失衡的证据。本研究利用一系列机理终点,包括线粒体呼吸和内皮抑制炎症、线粒体 DNA,研究了线粒体损伤在心脏毒性中的潜在参与。我们的研究提供了线粒体在内皮功能中作用的一些分子机制。在每一部分中,我们都试图介绍关键概念,然后分析以往研究揭示的线粒体功能障碍分子机制的重要性。我们的综述将针对线粒体蛋白功能的不同方面及其对内皮的影响和动脉粥样硬化疾病的原因。如今,为了评估健康的生活方式和线粒体平衡的更好状态,迫切需要利用适当的功能来达到治疗效果,这也是未来的发展方向。
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来源期刊
CiteScore
2.50
自引率
17.60%
发文量
114
审稿时长
6-12 weeks
期刊介绍: Molecular & Cellular Toxicology publishes original research and reviews in all areas of the complex interaction between the cell´s genome (the sum of all genes within the chromosome), chemicals in the environment, and disease. Acceptable manuscripts are the ones that deal with some topics of environmental contaminants, including those that lie in the domains of analytical chemistry, biochemistry, pharmacology and toxicology with the aspects of molecular and cellular levels. Emphasis will be placed on toxic effects observed at relevant genomics and proteomics, which have direct impact on drug development, environment health, food safety, preventive medicine, and forensic medicine. The journal is committed to rapid peer review to ensure the publication of highest quality original research and timely news and review articles.
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