Moreover, in vitro, differentially expressed miRs improved EC barrier formation (EV-miR-21) and rescued the angiogenic potential (HDL-miR-132) of ECs cultured in serum from patients with DM and DN.
Downregulation of miR-132-3p in alpha-cells of obese diabetic mice may constitute a compensatory mechanism contributing to keep glucagon-producing cell number constant in diabetes.
The findings of the present study suggested that increasing the expression of miR‑132 may serve as a novel therapeutic approach to inhibit the progression of cardiovascular disease in diabetes.