RCN1 downregulation-driven endoplasmic reticulum stress impairs endothelial function and diabetic foot ulcer healing.

ABSTRACT: Diabetic foot ulcers (DFUs) are a leading cause of disability and mortality, with endothelial dysfunction playing a key role in the development of non-healing ulcers. A primary driver of endothelial cell impairment in this context is endoplasmic reticulum (ER) stress, triggered by glycolipotoxicity, though the underlying mechanisms are not fully understood. In this study, we observed that diabetic mice displayed poor ulcer healing associated with reduced angiogenesis and downregulated Reticulocalbin 1 (RCN1) expression. Proteomic analysis in human umbilical vein endothelial cells (HUVECs) identified a strong link between RCN1 and the damaging effects of glycolipotoxicity on endothelial cell function, leading to impaired tubule formation, reduced migratory capacity, and increased apoptosis

SUBMITTER: Weng Z 

PROVIDER: S-EPMC12378791 | biostudies-literature | 2025 Aug

REPOSITORIES: biostudies-literature