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. 2026 Aug 24;17:1691999. doi: 10.3389/fphar.2026.1691999

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Copyright © 2026 Luo, Gao, Liang, Su, Liu, Ou, Zhang, Gao, Fu and Xie.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Complex scientific diagram illustrating the molecular pathways by which curcumin affects cardiac fibrosis and myocardial function, showing interactions between signaling molecules, cells, oxidative stress, apoptosis, fibrosis, and myocardial hypertrophy, supported by labeled arrows and explanatory icons. — Antifibrotic role of curcumin (CUR) in circulatory system fibrosis. CUR exerts multifaceted antifibrotic effects in the cardiovascular system by modulating inflammation, oxidative stress, autophagy, and extracellular matrix remodeling. Upward arrows (↑) indicate upregulation or activation, whereas downward arrows (↓) indicate downregulation or inhibition. CUR suppresses pro-inflammatory cytokine production and reduces inflammatory cell infiltration. It inhibits the transforming growth factor β (TGF-β)/Smad signaling pathway, downregulates pro-fibrotic mediators, and attenuates myofibroblast differentiation and endothelial–mesenchymal transition (EndMT). Autophagy is modulated by the regulation of LC3-II, Beclin-1, and autophagosome formation, with context-dependent effects on cardiac fibroblasts and cardiomyocytes. Additionally, CUR activates the NRF2/heme oxygenase 1 (HO-1) antioxidant axis, reduces NADPH oxidase-mediated oxidative stress, and inhibits MAPK/extracellular-regulated protein kinase (ERK) phosphorylation. Collectively, these coordinated actions reduce collagen deposition, suppress fibrosis, and improve cardiac function.