Mitochondrial Dysfunction: The Hidden Player in the Pathogenesis of Atherosclerosis?
Giovanni Ciccarelli1,2, Stefano Conte3, Giovanni Cimmino1,4
1Vanvitelli Cardiology Unit, Monaldi Hospital, 80131 Naples, Italy.
International Journal of Molecular Sciences
|January 21, 2023
Summary
Mitochondrial dysfunction contributes to atherosclerosis by impairing endothelial cells and increasing oxidative stress. Targeting mitochondria offers a promising therapeutic strategy for cardiovascular disease and aging.
Area of Science:
- Cardiovascular Biology
- Mitochondrial Medicine
- Aging Research
Background:
- Atherosclerosis is a complex inflammatory disease with residual cardiovascular risk despite therapeutic advances.
- Endothelial dysfunction and lipid accumulation drive atherosclerotic plaque development.
- Mitochondrial dysfunction in arterial cells elevates reactive oxygen species (ROS), promoting oxidative stress, inflammation, and lipid deposition.
Purpose of the Study:
- To explore the link between mitochondrial impairment and endothelial dysfunction in atherosclerosis and aging.
- To review current and novel mitochondria-targeting therapies for atherosclerosis.
Main Methods:
- Literature review focusing on data from multiple research groups.
- Analysis of the role of mitochondrial dysfunction in arterial wall cells.
- Examination of the impact of mitochondrial defects on endothelial function.
Main Results:
- Mitochondrial dysfunction is implicated in endothelial dysfunction, oxidative stress, and inflammation characteristic of atherosclerosis.
- Mitochondrial DNA (mtDNA) detection is key for assessing mitochondrial defects.
- Mitochondrial impairment contributes to atherosclerosis progression and aging.
Conclusions:
- Mitochondrial dysfunction is a critical factor in atherosclerosis and aging.
- Targeting mitochondria presents a novel therapeutic avenue for cardiovascular disease.
- Further research into mitochondria-based therapies is warranted for atherosclerosis treatment.
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