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. 2023 Jun 3;16(6):836. doi: 10.3390/ph16060836

Figure 4.

Figure 4

Schematic diagram representing cardioprotective molecular mechanisms of GLP-1 analogs in cardiomyocytes. The GLP-1R-dependent and -independent signaling pathways have been described as contributing to healthy myocardium and heart functions under pathophysiological conditions. The binding of GLP-1 to its receptor activates adenylate cyclase, and cAMP levels are elevated, which is followed by the activation of downstream cAMP sensitive molecular effectors in a GLP-1R-dependent way. While GLP-1R-independent GLP-1(9-36) activates PI3K, Akt, and the downstream signaling pathway, the full mechanisms of this process are not yet known. GLP-1, glucagon-like peptide-1; cAMP, cyclic adenosine monophosphate; Akt, protein kinase B; Epac, exchange protein activated by cAMP; CREB, cAMP-response element binding protein; CaMKKβ, calcium ions/calmodulins dependent protein kinase kinases β; PINK1, PTEN-induced kinase 1; Mfn, Mitofusin; Drp, dynamin-related protein; NF-κB, nuclear factor-κB; eNOS, endothelial nitric oxide synthase; AMPK, AMP-activated protein kinase; mTOR, mammalian target of rapamycin; ERK, extracellular-signal-regulated kinase; PI3K, phosphatidylinositide 3-kinase.