CoenzymeQ in cellular redox regulation and clinical heart failure.

Abstract Coenzyme Q (CoQ) is ubiquitously embedded in lipid bilayers of various cellular organelles. As a redox cycler, CoQ shuttles electrons between mitochondrial complexes and extramitochondrial reductases and oxidases. In this way, CoQ is crucial for maintaining the mitochondrial function, ATP synthesis, and redox homeostasis. Cardiomyocytes have a high metabolic rate and rely heavily on mitochondria to provide energy. CoQ levels, in both plasma and the heart, correlate with heart failure in patients, indicating that CoQ is critical for cardiac function. Moreover, CoQ supplementation in clinics showed promising results for treating heart failure. This review provides a comprehensive view of CoQ metabolism and its interaction with redox enzymes and reactive species. We summarize the clinical trials and applications of CoQ in heart failure and discuss the caveats and future directions to improve CoQ therapeutics.