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Salvianolic Acid B Inhibited LH2 Expression to Reduce Collagen Synthesis in Pulmonary Fibrosis
Songjun Shao1,2, Shanshan Rao2, Silu Hu1
1Department of Respiratory and Critical Care Medicine, State Key Laboratory of Respiratory Health and Multimorbidity, West China Hospital, Sichuan University, Chengdu, China.
Journal of Cellular and Molecular Medicine
|May 25, 2026
Summary
Salvianolic acid B (SAB) inhibits lysyl hydroxylase 2 (LH2) to reduce collagen cross-linking and lung scarring in pulmonary fibrosis. This offers a potential new treatment for fibrotic diseases.
Area of Science:
- Biochemistry
- Cell Biology
- Pathology
Background:
- Fibrotic diseases are characterized by excessive collagen deposition and scar formation.
- Lysyl hydroxylase 2 (LH2) is crucial for collagen cross-linking, enhancing matrix stiffness.
- Mechanisms regulating LH2 in pulmonary fibrosis (PF) remain incompletely understood.
Purpose of the Study:
- To investigate the role of LH2 in PF.
- To identify compounds targeting LH2-associated collagen cross-linking.
- To evaluate Salvianolic acid B (SAB) as a potential therapeutic agent for PF.
Main Methods:
- Assessed LH2 expression in PF models.
- Investigated the effect of LH2 silencing on fibrotic markers.
- Examined the impact of SAB on lung architecture, collagen deposition, and fibrotic pathways.
- Analyzed the modulation of epithelial-mesenchymal transition (EMT), fibroblast-to-myofibroblast transition (FMT), and Wnt/β-catenin signaling.
Main Results:
- LH2 expression was upregulated in PF, and its silencing reduced fibrotic protein expression.
- SAB treatment decreased LH2 levels, improved lung structure, and reduced collagen deposition.
- SAB and LH2 inhibition suppressed EMT, FMT, and the Wnt/β-catenin pathway.
Conclusions:
- Pharmacological inhibition of LH2 by SAB effectively disrupts collagen cross-linking.
- SAB demonstrates antifibrotic properties by targeting LH2 in pulmonary fibrosis.
- SAB represents a promising therapeutic strategy for treating pulmonary fibrosis.
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