Hilscher Moira, Hernandez-Gea Virginia, Friedman Scott L
Division of Liver Diseases, Mount Sinai School of Medicine, New York, NY, USA.
Biochim Biophys Acta. 2012 Jul;1831(7):972-8. doi: 10.1016/j.bbadis.2012.11.001. Epub 2012 Nov 9.
Autophagy is a catabolic pathway essential for cellular energy homeostasis that involves the self-degradation of intracellular components in lysosomes. This process has been implicated in the pathophysiology of many human disorders, including infection, cancer, and fibrosis. Autophagy is also recognized as a mediator of survival and proliferation, and multiple pathways induce autophagy under conditions of cellular stress, including nutrient and energy depletion. High autophagic activity has been detected in fibrogenic cells from several tissues; however the role of autophagy in fibrogenesis and mesenchymal cells varies greatly in different tissues and settings, with contributions uncovered to energy metabolism and collagen turnover by fibrogenic cells. Because several chemical modulators of autophagy have already been identified, autophagy regulation constitutes a potential target for antifibrotic therapy. This article is part of a Special Issue entitled: Fibrosis: Translation of basic research to human disease.
自噬是一种对细胞能量稳态至关重要的分解代谢途径,涉及溶酶体中细胞内成分的自我降解。这一过程与许多人类疾病的病理生理学有关,包括感染、癌症和纤维化。自噬也被认为是生存和增殖的介质,并且在细胞应激条件下,包括营养和能量耗竭时,多种途径可诱导自噬。在多个组织的成纤维细胞中已检测到高自噬活性;然而,自噬在纤维化和间充质细胞中的作用在不同组织和环境中差异很大,成纤维细胞对能量代谢和胶原蛋白周转的贡献已被揭示。由于已经鉴定出几种自噬的化学调节剂,自噬调节构成了抗纤维化治疗的一个潜在靶点。本文是名为:纤维化:基础研究向人类疾病的转化的特刊的一部分。