ArticleScientific reports2025
Allicin induced AMPK signaling attenuated Smad3 pathway mediated lung fibrosis.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Therapeutic Potential of Allicin in Multi-System Inflammatory Diseases.Current issues in molecular biology · 2026Review
- Sinigrin Mitigates Pulmonary Inflammation and Fibrosis Partly through Adenosine Monophosphate-Activated Protein Kinase (AMPK) Signaling.ACS pharmacology & translational science · 2026Article
- Inhalable Spray-Dried Carriers for Deep Lung Delivery and In Situ Synthesis of Allicin.ACS omega · 2026Article
- Trained Immunity Attenuates Bleomycin-Induced Pulmonary Fibrosis by Promoting AMPK-Mediated Autophagy in Alveolar Macrophages.Biology · 2026Article
- Advances in pharmacotherapy for fibrotic interstitial lung disease.Medical review (2021) · 2026Review
- Altered Metabolism in Idiopathic Pulmonary Fibrosis.Journal of cellular physiology · 2025Review
- Reversal of Myofibroblast Apoptosis Resistance and Collagen Deposition by Phaseoloidin-Induced Autophagy Attenuates Pulmonary Fibrosis.Biomedicines · 2025Article
- The Effect of Foliar Spraying of Different Selenium Fertilizers on the Growth, Yield, and Quality of Garlic (Plants (Basel, Switzerland) · 2025Article
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Authors and funding
16 authors.
Funding
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Abstract
Allicin, a natural compound derived from garlic, protects against oxidative stress-mediated tissue inflammation and vascular remodeling. Although these are key processes in lung fibrosis, the effects of allicin on this disease have never been evaluated. In this study, we aimed to evaluate the effects of allicin on lung fibroblast-mediated lung fibrosis and its mechanisms. We assessed the effects of allicin on fibronectin-mediated lung fibroblast migration and the contraction of three-dimensional type I collagen gels, and evaluated its anti-fibrotic effects in mice models of bleomycin (BLM)-induced lung fibrosis. The results showed that allicin suppressed transforming growth factor beta 1 (TGFβ1)-stimulated gel contraction and migration, as well as α-smooth muscle actin (α-SMA) and fibronectin. Additionally, allicin upregulated AMP-activated protein kinase (AMPK) phosphorylation, while suppressing Smad3 phosphorylation. An AMPK inhibitor further stimulated TGFβ1-induced gel contraction and migration. Furthermore, allicin suppressed BLM-induced lung fibrosis with suppressed Smad3 phosphorylation and BLM-induced lung injury with suppressed inflammatory cell infiltration in the mouse models. These results suggest that allicin may be a candidate therapeutic agent for suppressing the fibrotic phase mediated by pulmonary fibroblasts through upregulated AMPK resulting in suppressed Smad3 pathway after reducing the acute inflammatory phase.
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