Mechanistic insight of mitochondrial dysfunctions in cardiovascular diseases with potential biomarkers

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. 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. 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.