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.
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Schedule a callMore From: Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences
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