title: Pathophysiological role of autophagy: lesson from autophagy-deficient mouse models.
abstract: Autophagy is a cellular degradation system in which cytoplasmic components including organelles are sequestered by double membrane structures called autophagosomes and sequestered materials are degraded by lysosomal hydrolases for supply of amino acids and for cellular homeostasis. The autophagy induced in response to nutrient deprivation is executed in a nonselective fashion, and adaptation to nutrient-poor conditions is the main purpose of autophagy. On the other hand, recent studies have shed light on another indispensable role for starvation-independent or constitutive autophagy in cellular homeostasis, which is mediated by selective degradation of a specific substrate(s). Herein, we introduce pathophysiological roles of starvation-induced, constitutive, and selective autophagy (in particular, selective turnover of p62 through autophagy) disclosed by autophagy-deficient mouse models.
authors.affiliation: Protein Metabolism Project, Tokyo Metropolitan Institute of Medical ScienceSetagaya-ku, Tokyo 156-8501, Japan.
authors.forename: Yoshinobu
authors.initials: Y
authors.lastname: Ichimura
authors.forename: Masaaki
authors.initials: M
authors.lastname: Komatsu
mesh_terms: D000818:Animals; D001343:Autophagy; D002468:Cell Physiological Phenomena; D003593:Cytoplasm / Q000378:metabolism; D004195:Disease Models, Animal; D008247:Lysosomes / Q000378:metabolism; D051379:Mice; D008869:Microtubule-Associated Proteins / Q000378:metabolism; D010588:Phagosomes / Q000378:metabolism*; D012441:Saccharomyces cerevisiae / Q000502:physiology; D015398:Signal Transduction; D013217:Starvation / Q000503:physiopathology*; D051758:Transcription Factor TFIIH; D014157:Transcription Factors / Q000235:genetics / Q000502:physiology
chemical_list: C490981:Gtf2h1 protein, mouse; D008869:Microtubule-Associated Proteins; D014157:Transcription Factors; D051758:Transcription Factor TFIIH