ISSN 1016-5169 | E-ISSN 1308-4488
Archives of the Turkish Society of Cardiology
Effect of Mitochondrial Dysfunction on Coronary Artery Disease - Part 2 [Turk Kardiyol Dern Ars]
Turk Kardiyol Dern Ars. 2023; 51(3): 202-211 | DOI: 10.5543/tkda.2022.39448

Effect of Mitochondrial Dysfunction on Coronary Artery Disease - Part 2

Nazlı Doğan1, Neslihan Çoban2
1Istanbul University, Aziz Sancar Institute of Experimental Medicine, Department of Genetics, Istanbul, Türkiye
2İstanbul Üniversitesi, Sağlık Bilimleri Enstitüsü, İstanbul, Türkiye

Organelles whose functions change as a result of molecular processes are involved in the pathogenesis of atherosclerosis, which is the main cause of coronary artery disease, in addition to molecular processes. Recently, the role of mitochondria in the pathogenesis of coronary artery disease has attracted the attention of researchers. Mitochondria is a cell organelle with its own genome that plays a regulatory role in aerobic respiration, energy production, and cell metabolism. The number of mitochondria in cells changes dynamically, and there are different numbers of mitochondria in every tissue and every cell, depending on their function and energy needs. Oxidative stress causes mitochondrial dysfunction by leading to alterations in the mitochondrial genome and mitochondrial biogenesis. The dysfunctional mitochondria population in the cardiovascular system is closely related to the coronary artery disease process and cell death mechanisms. It is thought that the altered mitochondria (dys)function accompanying the molecular changes in the atherosclerosis process will be among the new therapeutic targets of coronary artery disease in the near future.

Keywords: Coronary artery disease, atherosclerosis, mitochondria, mitochondrial dysfunction

How to cite this article
Nazlı Doğan, Neslihan Çoban. Effect of Mitochondrial Dysfunction on Coronary Artery Disease - Part 2. Turk Kardiyol Dern Ars. 2023; 51(3): 202-211

Corresponding Author: Neslihan Çoban, Türkiye
Manuscript Language: Turkish


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