Figure 1: Schematic representation of the proposed pathways by which GLP-1 may exert its cardiovascular actions. The combination of GLP-1 effects on the myocardium (ie, apoptosis and necrosis prevention in cardiomyocytes through the activation of the RISK pathway, increased glucose metabolism, vasodilatory and anti-inflammatory actions) with GLP-1 metabolic and vascular effects at the systemic level contributes to cardiac survival and function improvement. cAMP: cyclic adenosine monophosphate; cGMP: cyclic guanosine monophosphate; Cyt c: cytochrome c; DPP-4: dipeptidyl peptidase-4; ERK: extracellular signal-regulated kinase; GLP-1: glucagon-like peptide-1; GLP-1R: GLP-1 receptor; GLUT: glucose transporter; GSK: glycogen synthase kinase; LDH: lactate dehydrogenase; MEK1/2: MAP kinase; MPTP: mitochondrial permeability transition pore; NOS: nitric oxide synthase; PI3K: phosphatidylinositol 3-kinase; PKA: protein kinase A; PKB: protein kinase B; ROS: reactive oxygen species. Reprinted with permission from Ravassa et al. Cardiovasc Res. 2012;94(2): 316–323 [37].