USP28 participates in high glucose-mediated endothelial dysfunction via deubiquitinating SIRT1 protein in diabetic foot ulcers.

ABSTRACT:

Background

Silent information regulator sirtuin 1 (SIRT1) protects and improves diabetic wound healing, but SIRT1 undergoes ubiquitination degradation in various cellular environments. The research aims to reveal a mechanism related to SIRT1 deubiquitination to attenuate HG-induced injury in human umbilical vein endothelial cells (HUVECs).

Methods

HUVECs treated with high glucose (HG) were utilized to simulate hyperglycemic conditions in vitro. Cell viability, proliferation, apoptosis, invasion, and angiogenesis were determined by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide, 5-ethynyl-2'-deoxyuridine, flow cytometry, transwell, and tube formation assays, respectively. Ferroptosis was analyzed by analyzing Fe²⁺ levels, reactive oxygen species

SUBMITTER: Liu Q 

PROVIDER: S-EPMC12462188 | biostudies-literature | 2025 Sep

REPOSITORIES: biostudies-literature