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Coenzyme Q10 (CoQ10) is a vital molecule present in cell membranes and mitochondria, existing in both its reduced (ubiquinol) and oxidized (ubiquinone) forms. Its levels are notably high in organs with high metabolic activity, such as the heart, kidneys, and liver, because it functions as an energy transfer molecule. However, CoQ10 levels can be reduced by factors such as aging, genetic predispositions, certain medications (e.g., statins), cardiovascular diseases (CVDs), degenerative muscle disorders, and neurodegenerative diseases. Due to its significant antioxidant and anti-inflammatory properties, CoQ10 helps prevent free radical-induced damage and the activation of inflammatory signaling pathways. Consequently, CoQ10 depletion can exacerbate inflammatory processes, making exogenous supplementation potentially beneficial as an adjunct treatment for cardiovascular diseases such as heart failure, atrial fibrillation, and myocardial infarction, as well as associated risk factors like hypertension, insulin resistance, dyslipidemias, and obesity.

CoQ10 was first identified by Frederick Crane in 1957. It is ubiquitously present in cell membranes and especially in mitochondria, where it participates in the electron transport chain in both its reduced and oxidized forms. Chemically, CoQ10 comprises a benzoquinone group and a poly-isoprenoid side chain, with the human variant being called CoQ10 due to its ten isoprenoid units. This molecule sustains continuous oxidation-reduction cycles, making it an excellent electron carrier. High concentrations of CoQ10 are found in organs such as the kidneys, heart, and liver, which require efficient energy transfer to support their high metabolic rates.

In the mitochondrial respiratory chain, CoQ10 transfers electrons from complex I (NADH-coenzyme Q reductase) or complex II (succinate-coenzyme Q reductase) to complex III (cytochrome c reductase). It also structurally supports complexes I and III, reducing the production of reactive oxygen species (ROS). CoQ10 accepts electrons from fatty acyl-coenzyme A dehydrogenases and is crucial in proton transport by uncoupling proteins, regulating mitochondrial permeability transition pores. Additionally, CoQ10 stabilizes calcium-dependent channels, regulates metabolism, influences cell signaling and growth, and locally regulates cytosolic redox intermediates like NADPH.

CoQ10, in its reduced form, inhibits the peroxidation of cell membrane lipids and reduces the oxidation of circulating lipids. It has been shown to inhibit low-density lipoprotein (LDL) oxidation more effectively than other antioxidants such as α-tocopherol or β-carotene. Most CoQ10 is synthesized within the cell, though the complete biosynthetic pathway is not fully understood. Recent research has revealed a biosynthetic complex for CoQ10 production in yeast and mammals, involving multiple mitochondrial uncharacterized proteins (MXPs) and several enzymes crucial to the CoQ10 pathway. The final, rate-limiting step occurs in the mitochondrial matrix, using 4-hydroxybenzoate as the quinone ring precursor from tyrosine and the isoprenoid tail from the mevalonate pathway, shared with cholesterol biosynthesis.

CoQ10 can also be obtained from the diet, with high levels found in fatty fish (salmon, sardines, tuna), soy, spinach, and nuts, though dietary intake is significant mainly in deficiency conditions. Factors such as aging, genetic predispositions, medications, and certain diseases can reduce plasma CoQ10 concentrations. Its depletion is linked to a greater propensity for immune inflammatory responses via the activation of processes like NF-κB gene expression. CoQ10’s potent antioxidant action helps prevent free radical damage by regulating transcriptional pathways and deactivating inflammatory pathways, making supplementation potentially effective in reducing inflammatory markers.

Given its critical role in bodily functions, CoQ10 deficiency is associated with various diseases and degenerative states, including cardiovascular disease, muscular dystrophy, Alzheimer’s disease, Parkinson’s disease, and others. While clinical evidence strongly supports CoQ10’s potential in cardiovascular health, further randomized controlled trials (RCTs) are needed to clarify its benefits in neurodegenerative diseases and other conditions such as cancer and muscular dystrophy.

This review aims to summarize the current evidence on using CoQ10 as an adjunct in treating cardiovascular disease patients, managing cardiovascular risk factors, and aiding statin-intolerant individuals, analyzing its impact on health and quality of life.

For more detailed information about this study.....