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NEDD4L-mediated RASGRP2 suppresses high-glucose and oxLDL-induced vascular endothelial cell dysfunctions by activating Rap1 and R-Ras.
Biochim Biophys Acta Mol Cell Res
December 2024
The Second Affiliated Hospital of Chongqing Medical University Cardiology Department, Chongqing, China. Electronic address:
Article Synopsis
- RASGRP2 is a crucial regulator of endothelial cell function, and its role in the progression of diabetes-related atherosclerosis is being explored for the first time.
- In experiments, low levels of RASGRP2 in endothelial cells exposed to high glucose and oxidized low-density lipoprotein were linked to increased cell permeability, apoptosis, and oxidative stress, while RASGRP2 overexpression showed protective effects.
- The study suggests that targeting the interaction between RASGRP2 and NEDD4L, or using modified exosomes from stem cells that overexpress RASGRP2, could provide effective strategies for addressing endothelial dysfunction in diabetic conditions.