ArticleJournal of translational medicine2026
Pirfenidone restores metabolic hormones and cardiac autophagy via p-AMPK in MASH.
Article in Journal of translational medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundObesity promotes chronic inflammation and insulin resistance, disrupting key metabolic hormones (e.g., insulin and leptin) and triggering metabolic dysfunction-associated steatohepatitis (MASH). Obesity is commonly associated with cardiovascular disease. Autophagy preserves heart function in response to various stresses. Pirfenidone (PFD) is an antifibrotic and anti-inflammatory drug. However, its effects on the regulation of metabolic hormones and cardiac autophagy in MASH have not been investigated.
methodsMale C57BL/6J mice were fed a high-fat/high-carbohydrate (HFHC) diet for 16 weeks to induce obesity and MASH. From week 8, a subgroup received PFD (300 mg/kg/day) via gavage. In vitro, H9c2 cardiomyocytes were exposed to glucolipotoxicity to simulate metabolic stress. Serum metabolic hormones, cardiac histology, microarray analysis, and autophagy-related mRNA and protein levels were analyzed.
resultsPFD treatment restored metabolic hormone balance and promoted cardiac autophagy in obese MASH mice. Mechanistically, PFD upregulated p-AMPK protein levels (P < 0.05), reversing the dysregulation of autophagy-related proteins both in vivo and in glucolipotoxicity-exposed H9c2 cells. Concurrently, PFD prevented systemic insulin resistance (P < 0.001), hepatic steatosis (P < 0.001), and liver damage (ALT/AST, P < 0.05). In cardiac tissue, PFD attenuated metabolic stress-induced hypertrophy (Nppa/Nppb mRNA), inflammation (Tnf, Il6, Adgre1, and Ccl2 mRNA, P < 0.05), and fibrosis (Tgfb1, Col1a1, and Col3a1 mRNA, P < 0.05).
conclusionsPirfenidone has cardioprotective effects in obesity-associated MASH by restoring metabolic hormone levels and activating autophagy via p-AMPK signaling. These findings suggest a potential translational therapeutic strategy for treating cardiovascular complications in MASH.
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