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The main mechanism of cardioprotective effects of GLP-1R agonists against oxidative stress-induced injury in H9c2 cells (cardiomyoblasts from Rattus norvegicus) and in cardiomyocytes is related to the scavenging of reactive oxygen species, by increasing the concentrations of endogenous antioxidant defenses and inhibiting cardiomyocyte apoptosis [42]

Thiele, A

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Interactions between DPP4 and the RAAS (including ACE2) have not been studied in detail but seem possible 74,75