Coenzyme Q10 Increases Cholesterol Efflux and Inhibits Atherosclerosis Through MicroRNAs

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Can coenzyme Q10 reduce the risk of side effects from statins?
 

 

Or is this  atherosclerosis inhibition a better reason for it?
Coenzyme Q10 Increases Cholesterol Efflux and Inhibits Atherosclerosis Through MicroRNAs

1. Ryan M. Allen,
2. Kasey C. Vickers

+ Author Affiliations

1. From the Department of Medicine, Vanderbilt University School of Medicine, Nashville, TN.

1. Correspondence to Kasey C. Vickers, PhD, Department of Medicine, Vanderbilt University School of Medicine, 2220 Pierce Ave 312B PRB, Nashville, TN 37232. E-mail kasey.c.vickers@vanderbilt.edu

Key Words:

• CoQ 10
• high-density lipoproteins
• microRNA

Atherosclerosis is a progressive inflammatory disease of the artery wall and the underlying basis for cardiovascular disease (CVD), which accounts for ≈32% of all deaths in the United States and is the leading cause of mortality in the world.¹ Atherosclerosis is classically defined by the accumulation of lipid and cholesterol deposits within the subendothelial space in the artery wall which leads to chronic inflammation and proinflammatory, cholesterol-laden macrophages which differentiate into resident foam cells in the lesion, ultimately forming an acellular necrotic core.² To date, the statin drug class has been overwhelmingly successful at reducing circulating total cholesterol levels, namely low-density lipoproteins cholesterol, the number one risk factor for CVD. Although pharmacological intervention with statins has dramatically reduced the number of cardiovascular events, many patients do not tolerate statins and a substantial disease burden remains even in patients who are on statins. Therefore, a great need remains to identify new drug targets and novel approaches to prevent and treat atherosclerosis and CVD. One strategy that has been extensively studied, but remains central to atherosclerosis reduction, is identifying new ways to increase the removal of excess cholesterol from peripheral cells and lesions through the reverse cholesterol transport (RCT) pathway. Briefly, the RCT pathway involves the transport of cholesterol from peripheral tissues (ie, foam cells within atherosclerotic lesions) to the liver by high-density lipoproteins (HDL), where cholesterol is excreted from the body as bile.³ This pathway is mediated by a number of lipid and cholesterol transporters, including the widely …

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