Bisdemethoxycurcumin attenuates myocardial fibrosis in heart failure with preserved ejection fraction by targeting TGFBR1 and oxidative stress
Abstract
models. The HFpEF mouse model was established using a high-fat diet and L-NAME. BDMC treatment improved cardiac function, attenuated myocardial fibrosis, and exhibited antioxidant effects. Mechanistically, integrated network pharmacology and proteomics identified TGFBR1 as a potential target. BDMC inhibited cardiac fibroblast activation by suppressing TGFBR1 expression and SMAD2/3 phosphorylation. Molecular docking and dynamics simulations confirmed stable binding between BDMC and TGFBR1. These findings demonstrate that BDMC mitigates myocardial fibrosis in HFpEF, primarily by competitively inhibiting the binding of TGF-β and TGFBR1, achieving the effect of inhibiting cardiac fibroblast activation.
Fields of Study & Subjects
Cardiac Fibrosis and Remodeling
Curcumin's Biomedical Applications
Cardiovascular Function and Risk Factors
Publication details
- Journal / source
- Computational and Structural Biotechnology Journal
- Publisher
- American Association for the Advancement of Science (AAAS)
- Volume
- 31
- Pages
- 422–435
- Publication date
- 1 January 2026
- Language
- EN