巨自噬/自噬主要负责细胞中受损细胞器和有毒大分子的降解。关于自噬维持细胞稳态的基本功能，自噬通量的变化或功能障碍可能导致疾病的发展。在本文中，评估了自噬在衰老相关病理和癌症中的复杂功能，强调了影响寿命和疾病发病机制的潜在分子机制。作为一种自然的生物过程，随着年龄的增长，自噬会减少，从而导致细胞损伤的积累和不同疾病的发展，包括神经系统疾病、心血管疾病和癌症。 MTOR、AMPK 和 ATG 蛋白在衰老过程中表现出变化，它们是有希望的治疗靶点。胰岛素/IGF1、TOR、PKA、AKT/PKB、热量限制和线粒体呼吸对于寿命调节至关重要，并且可以调节自噬或与自噬相互作用。特定类型的自噬，例如降解线粒体的线粒体自噬，可以通过影响这些细胞器并消除具有基因组突变的线粒体来调节衰老。自噬及其特定类型有助于癌发生的调节，并且能够双重增强或减少癌症进展。癌症标志，包括增殖、转移、治疗抵抗和免疫反应，均受到自噬的严格调控，支持自噬是癌症治疗中一个有前途的靶点的结论。版权所有 © 2024 Elsevier B.V. 保留所有权利。

Macroautophagy/autophagy is primarily accountable for the degradation of damaged organelles and toxic macromolecules in the cells. Regarding the essential function of autophagy for preserving cellular homeostasis, changes in, or dysfunction of, autophagy flux can lead to disease development. In the current paper, the complicated function of autophagy in aging-associated pathologies and cancer is evaluated, highlighting the underlying molecular mechanisms that can affect longevity and disease pathogenesis. As a natural biological process, a reduction in autophagy is observed with aging, resulting in an accumulation of cell damage and the development of different diseases, including neurological disorders, cardiovascular diseases, and cancer. The MTOR, AMPK, and ATG proteins demonstrate changes during aging, and they are promising therapeutic targets. Insulin/IGF1, TOR, PKA, AKT/PKB, caloric restriction and mitochondrial respiration are vital for lifespan regulation and can modulate or have an interaction with autophagy. The specific types of autophagy, such as mitophagy that degrades mitochondria, can regulate aging by affecting these organelles and eliminating those mitochondria with genomic mutations. Autophagy and its specific types contribute to the regulation of carcinogenesis and they are able to dually enhance or decrease cancer progression. Cancer hallmarks, including proliferation, metastasis, therapy resistance and immune reactions, are tightly regulated by autophagy, supporting the conclusion that autophagy is a promising target in cancer therapy.Copyright © 2024 Elsevier B.V. All rights reserved.