Mitochondrial and endothelial dysfunction is associated with several cardiovascular diseases

Many diseases of the heart and blood vessels, such as atherosclerosis, orArteriosclerosisIt is associated with mitochondrial and endothelial dysfunction in cardiovascular tissues. Despite the marked improvement in therapies for treating cardiovascular diseases, there is an unmet need to investigate mitochondria as a therapeutic target.

A recently published review explores the existing literature on relevant studies and makes recommendations for further study. The paper was written by Professor Giovanni Ciccarelli, an interventional cardiologist at Monaldi Hospital in Naples, Italy, and Associate Professor of Biology in the School of Science and Technology at Temple University. Co-authors include an international team working with the Sparrow Institute for Cancer Research and Molecular Medicine and the Sparrow Health Research Organization (SHRO), which is led by SHRO founder and president Antonio Giordano, MD, PhD, professor at Temple University and the University of Siena.

Article titled “Mitochondria Dysfunction: The Hidden Player in the Pathogenesis of Atherosclerosis?” appears in International Journal of Molecular Sciences. The authors suggest that close examination is necessary of this relationship between mitochondrial dysfunction, endothelial dysfunction, and atherosclerosis, to identify new precision medicine targets to better regulate mitochondrial functioning in patients with these conditions.

Mitochondrial dysfunction causes endothelial dysfunction due to a molecule called reactive oxygen species (ROS), or “free radicals,” which are produced by dysfunctional mitochondria. Then the increase in ROS leads to oxidative stress, inflammation, and the accumulation of cholesterol and lipids, leading to the formation of atherosclerotic plaques in the blood vessels.

Modulation of mitochondrial function through precision medicine can delay the progression of this endothelial dysfunction.

Despite the recognition of mitochondria as a novel therapeutic target in various disease contexts, no clinical or preclinical studies on atherosclerosis have been designed.

Both antioxidants and gene therapy are attractive approaches to treat atherosclerosis, however, more studies are needed.

The authors hope to initiate new clinical or preclinical trials to explore the effect of mitochondrial modulation on the progression of atherosclerotic plaque, in order to assess whether this type of therapeutic intervention can lead to a significant reduction in residual risks related to ischemic cardiovascular disease.

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