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The hepatic TGF-/Smad signaling pathway was downregulated by SEMA treatment, while sirtuin 1 (SIRT1) content and phosphorylated AMP-activated protein kinase (p-AMPK) expression were upregulated

Purpose of Review This review explores the rationale and available evidence behind incretin-based therapies for metabolic dysfunction-associated steatotic disease (MASLD) and metabolic-associated steatohepatitis (MASH), focusing on glucagon-like peptide 1 (GLP-1) and glucagon (GCG) receptor dual agonists (GLP-1/GCG RAs)
