| Literature DB >> 31102365 |
Shihao Zhao1, Xue Zhang1, Yuehai Ke1.
Abstract
Cellular senescence is a key factor driving age-related diseases. Recent studies have revealed that senescence-associated secretory phenotype, telomere attrition, epigenetic changes, and mitochondrial autophagy damage may mediate the pathogenesis of senescence-related idiopathic pulmonary fibrosis (IPF). Reducing the level of cellular senescence or clearing senescent cells can down-regulate the expression of fibrosis factors and alleviate the symptoms of IPF. In this review, we outlined the role and mechanism of cellular senescence in IPF.Entities:
Mesh:
Year: 2019 PMID: 31102365 PMCID: PMC8800647 DOI: 10.3785/j.issn.1008-9292.2019.02.16
Source DB: PubMed Journal: Zhejiang Da Xue Xue Bao Yi Xue Ban ISSN: 1008-9292