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The Use of Coenzyme Q10 in Cardiovascular Diseases

Journal

ANTIOXIDANTS
Volume 10, Issue 5, Pages -

Publisher

MDPI
DOI: 10.3390/antiox10050755

Keywords

Coenzyme Q10; ubiquinone; oxidative stress; heart failure; cardiac surgery; hypercholesterolemia; atherosclerosis; hypertension; endothelial dysfunction

Funding

  1. Consejeria de Educacion de la Junta de Comunidades de Castilla-La Mancha [SBPLY/19/180501/000245]
  2. Universidad de Castilla-LaMancha [2020-GRIN-29101]
  3. FEDER [2018/D/LD/MC/8]

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CoQ10, an endogenous antioxidant, plays a crucial role in energy metabolism and antioxidant protection in cardiovascular diseases. Clinical evidence shows that CoQ10 supplementation can reduce oxidative stress, mortality from cardiovascular causes, and improve the clinical outcome of patients.
CoQ10 is an endogenous antioxidant produced in all cells that plays an essential role in energy metabolism and antioxidant protection. CoQ10 distribution is not uniform among different organs, and the highest concentration is observed in the heart, though its levels decrease with age. Advanced age is the major risk factor for cardiovascular disease and endothelial dysfunction triggered by oxidative stress that impairs mitochondrial bioenergetic and reduces NO bioavailability, thus affecting vasodilatation. The rationale of the use of CoQ10 in cardiovascular diseases is that the loss of contractile function due to an energy depletion status in the mitochondria and reduced levels of NO for vasodilatation has been associated with low endogenous CoQ10 levels. Clinical evidence shows that CoQ10 supplementation for prolonged periods is safe, well-tolerated and significantly increases the concentration of CoQ10 in plasma up to 3-5 mu g/mL. CoQ10 supplementation reduces oxidative stress and mortality from cardiovascular causes and improves clinical outcome in patients undergoing coronary artery bypass graft surgery, prevents the accumulation of oxLDL in arteries, decreases vascular stiffness and hypertension, improves endothelial dysfunction by reducing the source of ROS in the vascular system and increases the NO levels for vasodilation.

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