{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Li C"],"funding":["Postgraduate Autonomous Exploration and Innovation Project of Central South University","National Natural Science Foundation of China","Natural Science Foundation of Hunan Province, China","Postgraduate Scientific Research Innovation Project of Hunan Province","Youth Foundation of Xiangya Hospital"],"pagination":["42"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9855167"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["12(1)"],"pubmed_abstract":["The senescence of vascular endothelial cells (ECs) is characterized as a hallmark of vascular aging, which leads to the initiation, progress, and advancement of cardiovascular diseases. However, the mechanism of the ECs senescence remains elusive. In this study, thoracic aortas were separated from young (8-week-old) and aged (18-month-old) mice. Decreased Ctsl expression and increased vascular remodeling were observed in senescent aorta. H<sub>2</sub>O<sub>2</sub> was used to induce human umbilical vein endothelial cells (HUVECs) senescence, as shown by increased SA-β-gal positive cells and upregulated p21 level. CTSV significantly decreased after H<sub>2</sub>O<sub>2</sub> treatment, while over-expression of CTSV by adenovirus reduced cellular senescence. RNA sequencing analysis was condu"],"journal":["Biology"],"pubmed_title":["Critical Role of Cathepsin L/V in Regulating Endothelial Cell Senescence."],"pmcid":["PMC9855167"],"funding_grant_id":["2022ZZTS0038","82000301","2020JJ5955","2017Q20","2021JJ40938","81800275","CX20220130","82170292"],"pubmed_authors":["Liu Z","Li C","Shi R","Chen M","Zhong H","Zhang L"],"additional_accession":[]},"is_claimable":false,"name":"Critical Role of Cathepsin L/V in Regulating Endothelial Cell Senescence.","description":"The senescence of vascular endothelial cells (ECs) is characterized as a hallmark of vascular aging, which leads to the initiation, progress, and advancement of cardiovascular diseases. However, the mechanism of the ECs senescence remains elusive. In this study, thoracic aortas were separated from young (8-week-old) and aged (18-month-old) mice. Decreased Ctsl expression and increased vascular remodeling were observed in senescent aorta. H<sub>2</sub>O<sub>2</sub> was used to induce human umbilical vein endothelial cells (HUVECs) senescence, as shown by increased SA-β-gal positive cells and upregulated p21 level. CTSV significantly decreased after H<sub>2</sub>O<sub>2</sub> treatment, while over-expression of CTSV by adenovirus reduced cellular senescence. RNA sequencing analysis was condu","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Dec","modification":"2025-04-04T11:33:20.92Z","creation":"2025-04-04T11:33:20.92Z"},"accession":"S-EPMC9855167","cross_references":{"pubmed":["36671735"],"doi":["10.3390/biology12010042"]}}