Senescent Cells in IPF: Locked in Repair?

Frontiers in Medicine

article

Silke Meiners¹  Mareike Lehmann² 

[1] Comprehensive Pneumology Center (CPC), Member of the German Center for Lung Research (DZL), University Hospital, Ludwig-Maximilians University;Research Unit Lung Repair and Regeneration, Member of the German Center for Lung Research (DZL)

关键词: senescence;    IPF;    IPF—idiopathic pulmonary fibrosis;    repair;    regeneration;   

DOI  :  10.3389/fmed.2020.606330

学科分类：社会科学、人文和艺术（综合）

来源: Frontiers

【 摘 要 】

Cellular senescence has been recognized since the 1960s as a cell biological program of aging. It also serves physiological functions in organismal development, regeneration and tissue repair. Senescence is triggered by replicative telomere attrition but also stress such as DNA damage, hypoxia, nutrient deprivation, mitochondrial impairment and oncogene activation (1, 2). In response to macromolecular damage, senescent cells enter a presumably permanent cell cycle arrest characterized by activation of the p53 DNA-damage response pathway and transcriptional induction of the cell cycle inhibitors p21WAF1/Cip and p16INK4A, which becomes reinforced by heterochromatin changes (3). Senescent cells are metabolically active, produce senescent-associated β-galactosidase and acquire a senescent-associated secretory phenotype (SASP) with secretion of pro-inflammatory cytokines, proteases and growth factors (3, 4).

【 授权许可】

CC BY