IGF2BP1-Mediates m6A Modification of KLF4 and Upregulates ADRM1 to Affect EndMT in Diabetic Atherosclerosis.
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Background: Atherosclerosis accelerates the progression of diabetes and metabolic syndrome. Endothelial to mesenchymal transition (EndMT) has been reported to promote the development of atherosclerosis and the generation of extracellular matrix. However, the mechanism of EndMT in diabetic atherosclerosis has not been fully clarified. Methods: A level. The effect of IGF2BP1 on the stability of KLF4 was detected by RNA stability assay. Wound healing and Transwell assays were used to detect HUVEC migration ability. Results: A level of KLF4. Functionally, IGF2BP1 upregulated KLF4 to promote HG combined with TGF-β1-induced EndMT in HUVECs. The results proved that IGF2BP1 regulated the KLF4/ADRM1 axis promoting EndMT in diabetic atherosclerosis. Conclusions: A modification of KLF4 and upregulated ADRM1 affect EndMT in diabetic atherosclerosis.
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