Endogenous Vasoactive Peptides and Vascular Aging-Related Diseases

Figure 10

The mechanisms of GLP-1 in protecting against vascular aging. GLP-1 is mainly secreted from intestinal L-cells and exerts its vascular protective effects by binding to its receptor GLP-1R expressed in the vessels. GLP-1 attenuated VSMC senescence, EC senescence, ECM remodeling, inflammation, and oxidative stress via activating multiple signaling pathways. Abbreviations: Akt: protein kinase B; AMPK: AMP-activated protein kinase; cAMP: cyclic adenosine monophosphate; CBP: CREB binding protein; EC: endothelial cell; ERK: extracellular regulated protein kinase; ECM: extracellular matrix; eNOS: endogenous nitric oxide synthase; GLP-1: glucagon-like peptide-1; KLF2: Krüppel-like factor 2; MMP: matrix metalloproteinase; NF-κB: nuclear factor kappa-B; Nrf2: nuclear factor-erythroid 2-related factor 2; PI3K: phosphatidylinositol 3 kinase; PKA: protein kinase A; RAGE: receptor for advanced glycation end products; ROCK: Rho associated coiled coil forming protein kinase; SIRT1: sirtuin1; VSMC: vascular smooth muscle cell.