Caloric restriction (CR) is the most common anti-aging intervention which can extend lifespan in organisms ranging from yeast to humans [81]. CR is a potent physiological activator of autophagy [82,83]. Several studies have demonstrated that autophagy is required for the CR-mediated lifespan extension [71,83]. Colman et al. [84] revealed that CR delayed the onset of many age-related pathologies, e.g. incidence of diabetes, cancer, cardiovascular disease and brain atrophy, as well as reducing the mortality of rhesus monkeys. Moreover, it is known that CR effectively protects against inflammatory responses and can combat age-related pro-inflammatory phenotype [85,86]. CR has also several beneficial effects on mitochondrial quality control, e.g. ROS production [87,88], which can improve cellular housekeeping and prevent inflammasomal activation. Many studies have indicated that mitochondrial quality control has a key role in the regulation of the aging process [89,90]. For instance, Trifunovic et al. [91] demonstrated that triggering of point mutations and deletions into mtDNA induced a premature aging phenotype in mice.
