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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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Diagram depicting the cellular and molecular mechanisms by which curcumin affects liver and pancreatic fibrosis. Section A illustrates signaling pathways in hepatocytes, emphasizing reduction of inflammation, oxidative stress, and extracellular matrix deposition. Section B summarizes curcumin’s modulation of epithelial cells, fibroblasts, and apoptosis, leading to prevention of fibrosis progression and hepatocyte disintegration. — Antifibrotic mechanisms of curcumin in liver fibrosis, oral submucous fibrosis (OSF), and pancreatic fibrosis. (A) Curcumin protects against liver and pancreatic fibrosis via multiple signaling pathways. Curcumin activates NRF2/Keap-1/heme oxygenase 1 (HO-1) and peroxisome proliferator-activated receptor-γ (PPARγ); inhibits MAPK/NF-κB/transforming growth factor β1 (TGF-β1)/Smad3 axes; reduces oxidative stress [reactive oxygen species (ROS) and malondialdehyde (MDA)], inflammation (TNF-α and IL-6), and fibrosis markers (α-SMA and collagen IA); and modulates apoptosis (Bax/Bcl-2) and autophagy (Beclin-1). These effects suppress hepatic stellate cell (HSC) activation, epithelial–mesenchymal transition (EMT), extracellular matrix (ECM) deposition, and hepatocyte disintegration. These mechanisms have been validated in models including carbon tetrachloride (CCl₄), thioacetamide (TAA), aflatoxin B1 (AFB1), bile duct-ligated (BDL), and others. Detailed molecular targets and clinical evidence are summarized in Supplementary Table S1. (B) Antifibrotic mechanisms of curcumin in OSF and pancreatic fibrosis.