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TAC-induced chronic stress resulted in substantial increases in myocardial hypertrophy (ANP and BNP mRNA levels) and cardiomyocyte cross-sectional area (CSA)

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Evidence has recently revealed that GLP-1RAs inhibit cardiac hypertrophy by upregulating GLP-1R expression and activating the AMPK/mechanistic target of the rapamycin (mTOR) signaling pathway [78]

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