Purpose of Review
Mitochondrial homeostasis and quality control are essential to maintenance of cardiac function and a disruption of this pathway can lead to deleterious cardiac consequences.
Mitochondrial quality control has been described as a major homeostatic mechanism in the cell. Recent studies highlighted that an impairment of mitochondrial quality control in different cell or mouse models is linked to cardiac dysfunction. Moreover, some conditions as aging, genetic mutations, or obesity have been associated with mitochondrial quality control alteration leading to an accumulation of damaged mitochondria responsible for increased production of reactive oxygen species, metabolic inflexibility, and inflammation, all of which can have sustained effects on cardiac cell function and even cell death.
In this review, we describe the major mechanisms of mitochondrial quality control, the factors that can impair mitochondrial quality control, and the consequences of disrupted mitochondrial quality control.