ArticleIranian journal of basic medical sciences2026
Imperatorin alleviates post-infarction cardiac fibrosis via the CD44/PI3K/AKT pathway in mice.
Article in Iranian journal of basic medical sciences, 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
Objectives: This study examines the effects of imperatorin (IMP) on cardiac fibrosis in mice with myocardial infarction (MI) and seeks to elucidate the underlying molecular mechanisms. Materials and Methods: C57BL/6 mice were randomly assigned to a control group, an ISO-induced MI group, and ISO+IMP treatment groups (7.5, 15, and 30 mg/kg). 4D-FastDIA-based quantitative proteomics was used for global proteomic analysis to identify differentially expressed proteins (DEPs) and signaling pathways involved in the anti-fibrotic effects of IMP following MI. Echocardiography was performed to evaluate cardiac function; histopathological analysis and serological indicators were used to assess myocardial injury; and Western blotting was employed to verify the expression and mechanisms of related proteins. Results: Compared with the ISO group, IMP treatment markedly improved electrocardiographic abnormalities, reduced serum LDH and cTn-I levels, enhanced cardiac function, and attenuated myocardial injury and fibrosis. Proteomic analysis identified 98 DEPs in the ISO/Control group and 127 DEPs in the ISO+IMP/ISO group. GO and KEGG analyses showed that these DEPs were mainly enriched in fibroblast proliferation-related biological processes and ECM-receptor interaction pathways, with significant involvement of the PI3K/AKT signaling pathway. PPI network analysis highlighted FN1, VTN, Colα2(I), Colα1(III), and CD44 as key regulatory proteins, among which CD44 was notably down-regulated by IMP. Molecular docking demonstrated strong binding affinity between IMP and CD44. Western blot results further confirmed that IMP significantly reduced the expression of fibrosis-related proteins and suppressed activation of the CD44/PI3K/AKT signaling pathway. Conclusion: IMP ameliorates myocardial fibrosis in MI mice by modulating the CD44/PI3K/AKT signaling pathway.
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