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The alterations of mitochondrial DNA in coronary heart disease

Haochang Hu1, Ying Lin1, Xiaofeng Xu1

  • 1School of Medicine, Ningbo University, Ningbo, Zhejiang, China.

Experimental and Molecular Pathology
|March 2, 2020
PubMed

Insights

Mitochondrial DNA (mtDNA) defects, including mutations and copy number changes, are linked to coronary heart disease (CHD). These alterations contribute to oxidative stress and energy deficits, impacting atherosclerosis and myocardial ischemia.

Area of Science:

  • Cardiovascular Science
  • Mitochondrial Biology
  • Genetics

Background:

  • Coronary heart disease (CHD) is a leading cause of mortality, characterized by atherosclerosis and potential ischemic events like myocardial infarction.
  • Mitochondria are vital for cellular energy production (ATP) via oxidative phosphorylation (OXPHOS).
  • Mitochondrial dysfunction, stemming from mitochondrial DNA (mtDNA) alterations, can lead to increased reactive oxygen species (ROS) and reduced ATP levels, promoting oxidative stress.

Purpose of the Study:

  • To review the role of mtDNA mutations, copy number variations, and haplogroups in the development and progression of CHD.
  • To highlight the potential of mtDNA defects as biomarkers for early diagnosis, prognosis, and therapeutic targets in atherosclerosis and CHD.

Main Methods:

  • Literature review synthesizing current research on mtDNA alterations and CHD.
  • Analysis of studies investigating the association between mtDNA mutations, copy number, haplogroups, and cardiovascular disease.
  • Examination of the mechanistic links between mitochondrial dysfunction and atherosclerotic processes.

Main Results:

  • mtDNA alterations (mutations, copy number changes, haplogroups) are associated with impaired OXPHOS function.
  • Mitochondrial dysfunction contributes to increased oxidative stress and reduced ATP production, exacerbating atherosclerosis.
  • These genetic and functional changes in mitochondria are implicated in the pathogenesis of CHD and myocardial ischemic injury.

Conclusions:

  • mtDNA defects are significant contributors to the pathophysiology of atherosclerosis and CHD.
  • mtDNA alterations offer potential for developing novel diagnostic, prognostic, and therapeutic strategies for CHD patients.
  • Further research into mtDNA's role is crucial for advancing cardiovascular medicine.

Keywords:
Altered copy number of mitochondrial DNAAtherosclerosisCoronary heart diseaseMitochondrial DNA mutationsReactive oxygen speciesmtDNA haplogroups

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