GLP-1 attenuated the endothelial dysfunction, the excessively stimulated autophagy of endothelial cells, and decreased the levels of ROS via reducing the phosphorylation of ERK 1/2 and restoring the expression of epigenetic factor histone deacetylase 6 (HDAC6), a key regulator of redox processes regulation [71]. This evidence concerns the gene GLP1R and endothelial dysfunction.