Effects of mitochondrial dysfunction on cellular function: Role in atherosclerosis

Biomed Pharmacother. 2024 May:174:116587. doi: 10.1016/j.biopha.2024.116587. Epub 2024 Apr 17.


Atherosclerosis, an immunoinflammatory disease of medium and large arteries, is associated with life-threatening clinical events, such as acute coronary syndromes and stroke. Chronic inflammation and impaired lipoprotein metabolism are considered to be among the leading causes of atherosclerosis, while numerous risk factors, including arterial hypertension, diabetes mellitus, obesity, and aging, can contribute to the development of the disease. In recent years, emerging evidence has underlined the key role of mitochondrial dysfunction in the pathogenesis of atherosclerosis. Mitochondrial dysfunction is believed to result in an increase in reactive oxygen species, leading to oxidative stress, chronic inflammation, and intracellular lipid deposition, all of which can contribute to the pathogenesis of atherosclerosis. Critical cells, including endothelial cells, vascular smooth muscle cells, and macrophages, play an important role in atherosclerosis. Mitochondrial function is also involved in maintaining the normal function of these cells. To better understand the relationship between mitochondrial dysfunction and atherosclerosis, this review summarizes the findings of recent studies and discusses the role of mitochondrial dysfunction in the risk factors and critical cells of atherosclerosis. FACTS: OPEN QUESTIONS.

Keywords: Apoptosis; Atherosclerosis; Mitochondrial dysfunction; Oxidative stress; ROS.

Publication types

  • Review

MeSH terms

  • Animals
  • Atherosclerosis* / metabolism
  • Atherosclerosis* / pathology
  • Endothelial Cells / metabolism
  • Endothelial Cells / pathology
  • Humans
  • Inflammation / metabolism
  • Inflammation / pathology
  • Macrophages / metabolism
  • Mitochondria* / metabolism
  • Mitochondria* / pathology
  • Muscle, Smooth, Vascular / metabolism
  • Muscle, Smooth, Vascular / pathology
  • Oxidative Stress* / physiology
  • Reactive Oxygen Species / metabolism
  • Risk Factors


  • Reactive Oxygen Species