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The present study aims to investigate whether semaglutide, a long-acting GLP1R agonist, can ameliorate cardiac hypertrophy induced by pressure overload, and explore the potential mechanism

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In contrast, real-world evidence suggests incremental benefits across MACE, heart failure, and renal outcomes, supporting the hypothesis that complementary mechanisms of action may translate into broader protection in clinical practice

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The bottleneck has two components: (1) the strength of GLP-1R activation (upstream), and (2) opposing calcium export mechanisms in the downstream protein network

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