ArticlePhysiological research2026
Pelargonidin Inhibits Isoproterenol Induced Myocardial Fibrosis via Regulating Transforming Growth Factor-beta/Smad2/3 Signaling and Th2 Cytokines in Mice.
Article in Physiological research, 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
Pelargonidin, a natural anthocyanidin, is known for its anti-inflammatory, antioxidant, and cytoprotective properties, however its role in myocardial fibrosis remains unclear. This study explored the therapeutic potential of pelargonidin in a mouse model of isoproterenol (ISO)-induced myocardial fibrosis. Male C57BL/6 mice were treated with ISO and subsequently administered either a low (20 mg/kg/day) or high (40 mg/kg/day) dose of pelargonidin, with captopril (15 mg/kg/day) serving as a reference control. Histological analysis revealed that pelargonidin significantly reduced collagen deposition in the myocardium in a dose-dependent manner. Molecular assessments showed decreased protein expression of alpha-SMA, COL3A1, and FN1, along with downregulation of TGF-beta/Smad2/3 signaling, as evidenced by reduced levels of TGF-beta and phosphorylated Smad2/3. Additionally, pelargonidin suppressed the expression of extracellular matrix-related genes and decreased circulating levels of Th2 cytokines IL-4 and IL-13. These findings indicate that pelargonidin mitigates myocardial fibrosis by targeting the TGF-beta/Smad2/3 pathway and modulating Th2-mediated immune responses. Overall, the results suggest that pelargonidin may serve as a promising therapeutic agent for myocardial fibrosis and related cardiovascular disorders. Key words Pelargonidin " Myocardial fibrosis " Transforming Growth Factor-beta " Extracellular matrix " Cytokines.
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41811698PMC13127988What Socratic holds
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