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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 biochemical pathway diagram illustrating the molecular mechanisms of curcumin in kidney protection, including modulation of mitochondrial function, inflammatory factors, oxidative stress, signaling pathways, and cellular outcomes, accompanied by labeled normal and degenerated kidney tubule illustrations. — Antifibrotic role of curcumin (CUR) in urinary system fibrosis. CUR protects against tubulointerstitial fibrosis through multiple interconnected pathways: (1) inhibiting epithelial–mesenchymal transition (EMT), (2) blocking transforming growth factor β (TGF-β)/Smad and MAPK signaling, (3) activating peroxisome proliferator-activated receptor-γ (PPARγ) and suppressing inflammation, (4) improving mitochondrial function and autophagy, (5) suppressing PI3K/AKT/mTOR and hypoxia-inducible factor 1α (HIF-1α)/vascular endothelial growth factor (VEGF) axes. These coordinated effects attenuate extracellular matrix (ECM) deposition, preserve the tubular structure, and promote DKD progression.