Role of autophagy in aging: The good, the bad, and the ugly

被引:53
作者
Tabibzadeh, Siamak [1 ,2 ]
机构
[1] Frontiers Biosci Res Inst Aging & Canc, Irvine, CA USA
[2] Frontiers Biosci Res Inst Aging & Canc, 16471 Sci Way, Irvine, CA 92618 USA
关键词
aging; AMPK; cancer; mTOR; SASP; senescence; CHAPERONE-MEDIATED AUTOPHAGY; BETA-CELL MASS; TARGETED DELETION; ER STRESS; SENESCENCE; ATG5; DISEASE; MECHANISMS; AGE; METABOLISM;
D O I
10.1111/acel.13753
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Autophagy (self-eating) is a conserved catabolic homeostatic process required for cellular metabolic demands by removal of the damaged molecules and organelles and for alleviation of stress initiated by pathology and infection. By such actions, autophagy is essential for the prevention of aging, disease, and cancer. Genetic defects of autophagy genes lead to a host of developmental, metabolic, and pathological aberrations. Similarly, the age-induced decline in autophagy leads to the loss of cellular homeostatic control. Paradoxically, such a valuable mechanism is hijacked by diseases, during tumor progression and by senescence, presumably due to high levels of metabolic demand. Here, we review both the role of autophagy in preventing cellular decline in aging by fulfillment of cellular bioenergetic demands and its contribution to the maintenance of the senescent state and SASP by acting on energy and nutritional sensors and diverse signaling pathways.
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页数:15
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