Abstract
Cardiovascular disease (CVD) is the leading cause of death in the world. The mechanism behind CVDs has been studied for decades; however, the pathogenesis is still controversial. Mitochondrial homeostasis plays an essential role in maintaining the normal function of the cardiovascular system. The alterations of any protein function in mitochondria may induce abnormal mitochondrial quality control and unexpected mitochondrial dysfunction, leading to CVDs. Posttranslational modifications (PTMs) affect protein function by reversibly changing their conformation. This review summarizes how common and novel PTMs influence the development of CVDs by regulating mitochondrial quality control. It provides not only ideas for future research on the mechanism of some types of CVDs but also ideas for CVD treatments with therapeutic potential.
Highlights
Cardiovascular disease (CVD) is currently one of the most perplexing diseases because of its variety and complexity
To make a better understanding of their roles in CVDs, we summarized the current research progress of several major posttranslational modifications (PTMs) that affect CVDs by regulating specific mitochondrial proteins which are closely implicated in mitochondrial quality control
Since most PTMs are reversible, it enables us to control the direction of each reaction by regulating different enzymes for the disease intervention based on their particular pathogenesis
Summary
Cardiovascular disease (CVD) is currently one of the most perplexing diseases because of its variety and complexity. Coronary artery disease is considered one of the major CVDs affecting the global human population and has been considered as a major cause of death in both developed and developing countries [3]. The pathologic process and risk factors of CVDs are still controversial, especially the molecular mechanisms on modulating mitochondria-associated proteins by posttranslational modifications (PTMs) [5, 6]. PTMs of proteins have been shown to affect mitochondrial quality control, thereby exacerbating or alleviating CVDs [17,18,19]. The purpose of this review is to summarize the functional changes of intracellular proteins especially mitochondrialrelated proteins by PTMs and their effects on CVDs, myocardial ischemia/reperfusion (I/R) injury, myocardial infarction, and heart failure. The PTMs including acetylation, phosphorylation, SUMOylation, ubiquitination, succinylation, lactylation, and crotonylation are discussed, and they shed light on a theoretical basis of CVD treatment in the future
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