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

FIGURE 2.

Infographic summarizing curcumin’s effects on pulmonary fibrosis (PF) mechanisms, displaying signaling pathways (TGF-β1/Smad, Nrf2/Keap-1/HO-1, NFκB, MAPK/ERK, JAK/STAT, p-ERK, PPARγ), resulting cellular processes (fibrosis, apoptosis, proliferation, migration), molecular mediators, and airway changes. Key molecules (COL, α-SMA, MMP, HYP) and cell types are color coded and illustrated with supporting icons and explanatory labels.

Multi-pathway regulatory network of curcumin against respiratory fibrosis. Curcumin exerts antifibrotic effects through coordinated modulation of multiple signaling pathways in pulmonary fibrosis, acute lung injury, and asthma models. The figure is organized in four layers: (1) inducers/insults [bleomycin (BLM), silica (SiO2), paraquat (PQ), irradiation, amiodarone, ovalbumin, and viral infection]; (2) core signaling pathways [transforming growth factor β (TGF-β)/Smad, NRF2/heme oxygenase 1 (HO-1), NF-κB, JAK/STAT, MAPK/extracellular-regulated protein kinase (ERK), p-ERK, and peroxisome proliferator-activated receptor-γ (PPARγ)]; (3) cellular events [fibroblast proliferation/migration/differentiation and alveolar epithelial cell apoptosis/epithelial–mesenchymal transition (EMT)/autophagy]; and (4) antifibrotic outcomes (reduced collagen deposition, hydroxyproline, matrix metalloproteinase (MMP)-2/9, inflammatory infiltration, and fibrotic area). The black solid arrows (→) indicate the flow of signaling and pathological events, the symbol (⊣) denotes inhibition or blockade, and the red upward arrows (↑) and green downward arrows (↓) exclusively indicate the upregulation and downregulation of molecular expression, respectively. The dashed lines indicate pathways with cell type-specific or context-dependent effects. For a comprehensive list of regulated molecules and corresponding references, please refer to Table 1.