Cathepsin L induces cellular senescence by upregulating CUX1 and p16^INK4a.

ABSTRACT: Cathepsin L (CTSL) has been implicated in aging and age-related diseases, such as cardiovascular diseases, specifically atherosclerosis. However, the underlying mechanism(s) is not well documented. Recently, we demonstrated a role of CUT-like homeobox 1 (CUX1) in regulating the p16^INK4a-dependent cellular senescence in human endothelial cells (ECs) and vascular smooth muscle cells (VSMCs) via its binding to an atherosclerosis-associated functional SNP (fSNP) rs1537371 on the CDKN2A/B locus. In this study, to determine if CTSL, which was reported to proteolytically activate CUX1, regulates cellular senescence via CUX1, we measured the expression of CTSL, together with CUX1 and p16^INK4a, in human ECs and VSMCs undergoing senescence. We discovered that CUX1 is not

SUBMITTER: Wu Y 

PROVIDER: S-EPMC11272106 | biostudies-literature | 2024 Jun

REPOSITORIES: biostudies-literature