Abstract
The incidence rate of cardiovascular disease (CVD) has been increasing year by year and has become the main cause for the increase of mortality. Mitochondrial DNA (mtDNA) plays a crucial role in the pathogenesis of CVD, especially in heart failure and ischemic heart diseases. With the deepening of research, more and more evidence showed that mtDNA is related to the occurrence and development of CVD. Current studies mainly focus on how mtDNA copy number, an indirect biomarker of mitochondrial function, contributes to CVD and its underlying mechanisms including mtDNA autophagy, the effect of mtDNA on cardiac inflammation, and related metabolic functions. However, no relevant studies have been conducted yet. In this paper, we combed the current research status of the mechanism related to the influence of mtDNA on the occurrence, development, and prognosis of CVD, so as to find whether these mechanisms have something in common, or is there a correlation between each mechanism for the development of CVD?
Highlights
Introduction of Mitochondrial DNA (mtDNA) Structure andFunction [1] mtDNA itself is a small, double-stranded circular molecule, and human mtDNA is 16,569 bp in length. mtDNA encodes 13 polypeptide subunits of the oxidative phosphorylation (OXPHOS) enzyme complexes, 22 transfer RNAs, and 2 ribosome RNAs, which are needed for mitochondrial respiration [2]
It is clear that mtDNA plays an important role in keeping mitochondria normal (Table 1)
The copy number of mtDNA can reflect the occurrence and development of cardiovascular disease (CVD) to some extent. mtDNA damage causes a variety of related metabolic diseases in human body and is an important point of CVD and causes of new coronary CVD. mtDNA is special due to its composition and structure, such as no histone protection and located near the respiratory chain, the main site of endogenous oxygen radicals
Summary
Studies had shown that acute myocardial infarction can cause aseptic inflammation, aggravate tissue damage, and lead to increased levels of mtDNA, which activates the NF-κB pathway through TLR9 and triggers an innate immune response, leading to myocardial cell damage. In heart failure following ischemic heart injury, a strong inflammatory response leads to further injury and dysfunction of cardiac contraction and expansion, and the release of cell debris during tissue injury causes conformational changes in NLRP3 inflammasomes, leading to the activation of caspase.Clinical treatment of heart failure patients with IL-1 antagonist injection showed increased oxygen consumption, which is expected to be a new direction of heart failure treatment in the future. The inflammatory response increased significantly, often accompanied by chronic inflammation, which is caused by abnormal responses to TLR92, TLR12, NLRP35, and/or cGAS-STING13, triggering the occurrence and development of CVD [38].
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