关键词： AEN AMP-activated protein kinase AMPK BCL2/adenovirus E1B 19kDa interacting protein 3 BECN1 BNIP3 Beclin 1 Cancer DAPK1 DNA-damage regulated autophagy modulator 1 DRAM1 EGFR EIF2AK3 FOXO HIF-1 HSF1 IGFBP3 IKK IκB IκB kinase JAK Janus kinase MAP1LC3 MAPK MEF Mitophagy NF-κB-inducing kinase NIK NLS PAMP PI3K PINK1 PKR PTEN PTEN-induced putative kinase 1 RB1-inducible coiled-coil protein 1 RB1CC1 REL homology domain RHD SQSTM1 STAT3 TAB TAK1 TAK1-binding protein TIGAR TNF TNF receptor 1 TNFR1 TP53-induced glycolysis and apoptosis regulator TSC2 apoptosis enhancing nuclease death-associated protein kinase 1 eIF2α epidermal growth factor receptor eukaryotic translation initiation factor 2α eukaryotic translation initiation factor 2α kinase 3 forkhead box O heat shock transcription factor 1 hypoxia-inducible factor 1 inhibitor of κB insulin-like growth factor-binding protein 3 mTOR mammalian target of rapamycin microtubule-associated protein 1 light chain 3 mitogen-activated protein kinase mouse embryonic fibroblast nuclear localization signal pathogen-associated molecular pattern phosphatase and tensin homolog phosphoinositide-3-kinase protein kinase, RNA-activated sequestosome 1 signal transducer and activator of transcription 3 transforming growth factor β-activated kinase 1 tuberous sclerosis 2 tumor necrosis factor

Mesh ： Animals Autophagy / physiology Humans Protein Processing, Post-Translational Signal Transduction Stress, Physiological / physiology Transcription Factors / metabolism

来  源：   DOI：10.1016/j.semcancer.2013.05.008   PDF(Sci-hub)

Abstract：
Autophagy is an evolutionarily conserved process that promotes the lysosomal degradation of intracellular components including organelles and portions of the cytoplasm. Besides operating as a quality control mechanism in steady-state conditions, autophagy is upregulated in response to a variety of homeostatic perturbations. In this setting, autophagy mediates prominent cytoprotective effects as it sustains energetic homeostasis and contributes to the removal of cytotoxic stimuli, thus orchestrating a cell-wide, multipronged adaptive response to stress. In line with the critical role of autophagy in health and disease, defects in the autophagic machinery as well as in autophagy-regulatory signaling pathways have been associated with multiple human pathologies, including neurodegenerative disorders, autoimmune conditions and cancer. Accumulating evidence indicates that the autophagic response to stress may proceed in two phases. Thus, a rapid increase in the autophagic flux, which occurs within minutes or hours of exposure to stressful conditions and is entirely mediated by post-translational protein modifications, is generally followed by a delayed and protracted autophagic response that relies on the activation of specific transcriptional programs. Stress-responsive transcription factors including p53, NF-κB and STAT3 have recently been shown to play a major role in the regulation of both these phases of the autophagic response. Here, we will discuss the molecular mechanisms whereby autophagy is orchestrated by stress-responsive transcription factors.
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