The physiological roles of autophagy in the mammalian life cycle

Abstract

Autophagy is primarily an efficient intracellular catabolic pathway used for degradation of abnormal cellular protein aggregates and damaged organelles. Although autophagy was initially proposed to be a cellular stress responder, increasing evidence suggests that it carries out normal physiological roles in multiple biological processes. To date, autophagy has been identified in most organs and at many different developmental stages, indicating that it is not only essential for cellular homeostasis and renovation, but is also important for organ development. Herein, we summarize our current understanding of the functions of autophagy (which here refers to macroautophagy) in the mammalian life cycle.

Identification of a novel autophagy-related gene signature for predicting metastasis and survival in patients with osteosarcoma

“…GO results showed that the BP of DEARGs mainly involved autophagy, macroautophagy, autophagosome assembly, autophagosome organization, and autophagy of mitochondrion; the CC were mainly enriched in autophagosome, phagophore assembly site, autophagosome membrane, vacuolar membrane, and late endosome; and the MF mainly involves ubiquitin protein ligase binding, chaperone binding, protein serine/ threonine kinase activity, and heat shock protein binding. Previous studies have shown that autophagy [33], macroautophagy [10], autophagosome [34] BECN1, ATG7, ATG12, PIK3C3, GABARAP, GABARAPL1, GABARAPL2, MAP1LC3A, MAP1LC3B, and SQSTM1 are the hub autophagy-related genes identified in this study. BECN1 affects the drug sensitivity of OS cells by mediating the autophagy process [43].…”

“…Autophagy is a highly conserved intracellular degradation pathway that maintains homeostasis by degrading intracellular macromolecules and organelles through the formation of autophagosomes and subsequent fusion with lysosomes [6,7]. Autophagy is widely involved in the physiological and pathological processes of cells in vivo, such as cell homeostasis, hematopoiesis, organ development, neurodegeneration, and tumorigenesis [8][9][10]. Basal levels of autophagy are employed by cells under normal circumstances.…”

“…Basal levels of autophagy are employed by cells under normal circumstances. When cells become deficient in nutrition or are exogenously stimulated, their autophagy levels increase accordingly to cope with unfavorable factors, as an adaptive response to metabolic stress [10]. Many studies have shown that autophagy could promote or inhibit the survival of tumor cells at different stages of cancer development [11].…”

Quinoline‐Conjugated Ruthenacarboranes: Toward Hybrid Drugs with a Dual Mode of Action

“…For the present work, we were particularly interested in the activity of substituted quinolines as modulators of macroautophagic processes, often simply called autophagy. The latter is an ensemble of physiologic catabolic processes, which break cytosolic proteins and organelles down to their building blocks, e. g. amino acids, in response to a plethora of stressors including starvation, oxidative stress and pathogens, and act also as a quality control system, to ensure homeostatic functions and organelle turnover. Strong evidence has been collected in the last 20 years which supports a dual role of autophagy in cancer, either in tumor suppression or in tumor promotion, depending on the specific cancer type and the stage .…”

Autophagy-Dependent Reactivation of Epstein-Barr Virus Lytic Cycle and Combinatorial Effects of Autophagy-Dependent and Independent Lytic Inducers in Nasopharyngeal Carcinoma

“…In a previous study, we have characterized the mode of action of a novel compound, C7, that reactivates EBV lytic cycle via intracellular iron chelation and activation of the ERK1/2-autophagy axis [6]. Given that autophagy is a conserved cellular mechanism for maintaining cellular homeostasis and plays an essential role in governing cell death and survival [7][8][9], we endeavor to further delineate the role of autophagy in EBV lytic reactivation.…”