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One such study found that GLP-1 elevates intracellular cAMP, subsequently activating protein kinase A (PKA), which in turn inhibits RhoA/ROCK signaling, resulting in the disassembly of glucotoxicity-induced stress fibers 6

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A PubMed-indexed study on GLP-1R agonist design used in vitro and in vivo assays to compare signaling characteristics against Semaglutide as a reference compound

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