| Literature DB >> 33864479 |
Xue Li1, Fuxiaonan Zhao2, An Wang2, Peiyong Cheng1, Huaiyong Chen3,4,5,6.
Abstract
Mammalian lungs are metabolically active organs that frequently encounter environmental insults. Stress responses elicit protective autophagy in epithelial barrier cells and the supportive niche. Autophagy promotes the recycling of damaged intracellular organelles, denatured proteins, and other biological macromolecules for reuse as components required for lung cell survival. Autophagy, usually induced by metabolic defects, regulates cellular metabolism. Autophagy is a major adaptive response that protects cells and organisms from injury. Endogenous region-specific stem/progenitor cell populations are found in lung tissue, which are responsible for epithelial repair after lung damage. Additionally, glucose and fatty acid metabolism is altered in lung stem/progenitor cells in response to injury-related lung fibrosis. Autophagy deregulation has been observed to be involved in the development and progression of other respiratory diseases. This review explores the role and mechanisms of autophagy in regulating lung metabolism and epithelial repair.Entities:
Keywords: Asthma; COPD; Epithelial stem cells; Glycolysis; Idiopathic pulmonary fibrosis; Lung regeneration
Year: 2021 PMID: 33864479 DOI: 10.1007/s00018-021-03841-7
Source DB: PubMed Journal: Cell Mol Life Sci ISSN: 1420-682X Impact factor: 9.261