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By pharmacological approaches, we further showed that a distinct G s /cAMP-protein kinase A (PKA)/inositol 1,4,5-trisphosphate (IP 3 )/Ca 2+ /calmodulin (CaM)/CaM-dependent protein kinase II (CaMKII) signaling pathway is responsible for the exendin-4 effect on GCs

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Rodents overexpressing USP22 or lncRNA PART1 were well resistant to I/R-induced oxidative stress and cardiac injury, which may be partly attributed to the elevated GSH content in the myocardium [251, 252]

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