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.

中文翻译：

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具有潜在生物标志物的心血管疾病线粒体功能障碍的机制见解

背景

动脉粥样硬化形成的加速是心血管疾病 (CVD) 的后果，心血管疾病 (CVD) 是由线粒体功能障碍 (MD) 引起的。内皮抑制炎症、修复以及与附近组织的液体交换。内皮介导的线粒体损伤可以触发微血管内皮层血管舒张、促炎症和促血栓积累过程的分子机制。脂质颗粒的氧化产生修饰的脂蛋白。线粒体功能的改变最近引起了动脉粥样硬化引发和进展的极大关注，因为线粒体突变可以将线粒体DNA释放到细胞质中，并且可以作为病毒DNA或外源DNA的传感器。另一个原因是线粒体失衡会导致产生过量的活性氧（ROS），从而导致细胞代谢和呼吸系统。

目标

以往的一些研究表明，线粒体功能障碍在心脏病中起着至关重要的作用。然而，很少有研究提供内皮介导的线粒体失衡的证据。本研究使用一系列机制终点（包括线粒体呼吸和炎症、线粒体 DNA 的内皮抑制）研究了线粒体损伤在心脏毒性中的潜在参与。我们的研究提供了一些有关线粒体在内皮功能中作用的分子机制。在每个部分中，我们都试图介绍关键概念，然后分析之前的研究揭示了线粒体功能障碍分子机制的重要性。

结论

我们审查的最终目标是找出新的药物发现或新的治疗方法。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细胞的影响和动脉粥样硬化疾病的原因。为了评估当今健康的生活方式和更好的线粒体平衡状况，迫切需要利用适当的功能来达到治疗效果，为未来的方向提供帮助。