SYSTEMATIC REVIEW article
Front. Med.
Sec. Pulmonary Medicine
Emodin for pulmonary fibrosis: a systematic review and meta-analysis of efficacy and molecular mechanisms
Provisionally accepted
- Changchun University of Chinese Medicine, Changchun, China
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Objective This systematic review and meta-analysis aimed to evaluate emodin's therapeutic efficacy in animal models of pulmonary fibrosis (PF) and summarize its anti-fibrotic mechanisms, providing a theoretical basis for the application of emodin in the clinical treatment of fibrosis. Methods A comprehensive literature search was conducted across 4 major international databases and 4 Chinese databases through July 2025. Study quality was assessed using the SYRCLE risk of bias tool. The mean difference (MD) or standardized mean difference (SMD) with 95% confidence intervals (CIs) was used to evaluate emodin's effects on fibrosis severity, histopathological damage, inflammation, oxidative stress, and epithelial-mesenchymal transition (EMT). Results Meta-analysis revealed emodin significantly attenuated PF across multiple scales [Szapiel score: SMD = −1.73, 95% CI: −2.02 to −1.43; Ashcroft score: SMD = −3.10, 95% CI: −4.40 to −1.79; fibrotic area: SMD = −4.97, 95% CI: −7.87 to −2.08]. Emodin substantially reduced hydroxyproline content (SMD = −1.91, 95% CI: −2.42 to −1.41) and collagen deposition, while improving alveolitis (SMD = −1.89, 95% CI: −2.21 to −1.57) and lung coefficients (SMD = −1.35, 95% CI: −2.06 to −0.65). Emodin also mitigated inflammation by reducing pulmonary levels of IL-6 (SMD = −3.86, 95% CI: −6.21 to −1.51), IL-1β (SMD = −3.21, 95% CI: −4.90 to −1.53), and TNF-α (SMD = −3.31, 95% CI: −3.96 to −2.67). Additionally, it attenuated oxidative stress and inhibited EMT by elevating SOD activity (SMD = 4.69, 95% CI: 3.59 to 5.80) while decreasing MDA (SMD = −3.58, 95% CI: −4.48 to −2.68) and TGF-β levels (SMD = −2.72, 95% CI: −3.41 to −2.02). This is a provisional file, not the final typeset article Conclusion Emodin effectively alleviates PF through reducing collagen deposition, attenuating inflammation, suppressing oxidative stress, and inhibiting EMT. Subgroup analyses indicated that heterogeneity across studies was partly attributable to variations in dosing regimens and animal species. Further investigation into the anti-fibrotic properties of emodin is warranted to facilitate its therapeutic development.
Keywords: Emodin, Pulmonary Fibrosis, Animal Models, Inflammation, Oxidative Stress, Meta-analysis
Received: 28 Oct 2025; Accepted: 19 Nov 2025.
Copyright: © 2025 Zhou, Sima, Fang, Cui, Han, Wang, Liu, Bi and Yue. 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) or licensor 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.
* Correspondence: Donghui Yue, yuedonghui7776@outlook.com
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