The aging process involves a progressive decline in cellular and organismal function. The major hallmark of aging is the deficient maintenance of proteostasis which permits the accumulation of damaged and defective cellular components, e.g. lipofuscin, within cells. Brunk and Terman [66] called this cellular status as “garbage can” hypothesis of aging. They proposed that lipofuscin accumulation would disturb lysosomal degradation thus inhibiting the cleansing of dysfunctional mitochondria. After ten years of experimental work, this hypothesis still seems to be valid since different research approaches have demonstrated that autophagy clearly declines with aging and the number of dysfunctional mitochondria augments. In particular, defects in mitochondrial uptake and degradation could increase ROS production and stimulate inflammasomes. Recently, this research topic has been extensively reviewed in detail elsewhere [67-72].
