Atherosclerosis and Coenzyme Q10

Abstract

Atherosclerosis is the most common cause of cardiac deaths worldwide. Classically, atherosclerosis has been explained as a simple arterial lipid deposition with concomitant loss of vascular elasticity. Eventually, this condition can lead to consequent blood flow reduction through the affected vessel. However, numerous studies have demonstrated that more factors than lipid accumulation are involved in arterial damage at the cellular level, such as inflammation, autophagy impairment, mitochondrial dysfunction, and/or free-radical overproduction. In order to consider the correction of all of these pathological changes, new approaches in atherosclerosis treatment are necessary. Ubiquinone or coenzyme Q10 is a multifunctional molecule that could theoretically revert most of the cellular alterations found in atherosclerosis, such as cholesterol biosynthesis dysregulation, impaired autophagy flux and mitochondrial dysfunction thanks to its redox and signaling properties. In this review, we will show the latest advances in the knowledge of the relationships between coenzyme Q10 and atherosclerosis. In addition, as atherosclerosis phenotype is closely related to aging, it is reasonable to believe that coenzyme Q10 supplementation could be beneficial for both conditions.

CoenzymeQ10-Induced Activation of AMPK-YAP-OPA1 Pathway Alleviates Atherosclerosis by Improving Mitochondrial Function, Inhibiting Oxidative Stress and Promoting Energy Metabolism

“…Recent studies have found that atherosclerosis is closely related to aging. At the same time, factors such as inflammation, autophagy damage, mitochondrial dysfunction and excess free radicals more closely influence the development of atherosclerosis at the cellular level ( Suárez-Rivero et al, 2019 ). As a kind of electron transfer, CoQ10 can transfer electrons from mitochondrial respiratory chain compound I (NADH ubiquinone oxidoreductase) and compound II (Ubiquinone succinate oxidoreductase) to the compound III (Ubiquinone cytochrome c reductase).…”

Implication of nuclear factor‐erythroid 2‐like 2/heme oxygenase 1 pathway in the protective effects of coenzyme Q10 against preeclampsia‐like in a rat model

“…10 Given the crucial role of coenzyme Q10 in the MRC and other mitochondrial functions, the abnormal absence of coenzyme Q10 leads to various clinical defects including hypertension, metabolic diseases, and atherosclerosis. 21,22 The therapeutic potential of coenzyme Q10 has been widely studied. 23 Recent researches have revealed the therapeutic potential of coenzyme Q10 in a variety of diseases.…”

“…Coenzyme Q10 is a form of fat‐soluble ubiquinone in human and is mainly located in the mitochondria 10 . Given the crucial role of coenzyme Q10 in the MRC and other mitochondrial functions, the abnormal absence of coenzyme Q10 leads to various clinical defects including hypertension, metabolic diseases, and atherosclerosis 21,22 . The therapeutic potential of coenzyme Q10 has been widely studied 23 .…”

Enhancer of zeste homolog 2 participates in the process of atherosclerosis by modulating microRNA‐139‐5p methylation and signal transducer and activator of transcription 1 expression

“…2 AS is the most familiar cause of cardiac deaths around the world. 3 A plenty of pathological events, consisting of migration and proliferation of endothelial cells and vascular smooth muscle cells, lipid deposition and persistent inflammation, and oxidative stress are implicated in the development of AS. 4,5 Some characteristics of atherogenesis, including strengthened vascular permeability, the expression of adhering molecules in endothelial cells, the increase of inflammatory monocytesor macrophages, and the expression of proteases are applied for therapy of AS.…”