ArticleFrontiers in pharmacology2025
Resveratrol attenuates pulmonary fibrosis by inhibiting alveolar epithelial senescence via targeting SASP-related proteins: an integrated bioinformatics-experimental study.
Article in Frontiers in pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- Progress on the mechanism of Piezo1 in mechanical ventilation-induced lung injury.Journal of thoracic disease · 2026Review
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Authors and funding
10 authors.
Funding
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Abstract
Background: Pulmonary fibrosis (PF) is a progressive and fatal interstitial lung disease with limited treatment options. Premature senescence of alveolar epithelial type II cells (AT2 cells) plays a critical role in PF pathogenesis. This study aimed to identify natural compounds targeting senescence-related pathways for PF treatment. Methods: An integrated approach was implemented, combining bioinformatics, artificial intelligence (AI)-assisted molecular docking, ADMET (absorption, distribution, metabolism, excretion, and toxicity) profiling, and experimental validation. Core targets associated with aging-related pulmonary fibrosis (PF) were identified via database mining (GeneCards and AgingAtlas) and protein-protein interaction (PPI) network analysis. Natural compounds were screened using the HERB database, and resveratrol (RES) was selected due to its multi-target activity and favorable ADMET characteristics. The efficacy of RES was evaluated through Results: Bioinformatics identified 322 aging-related PF targets, with TP53, AKT1, STAT3, JUN, and NFKB1 as core regulators. Resveratrol was selected as a top candidate modulating all five core targets and exhibiting optimal drug-likeness. Molecular docking and dynamics simulations confirmed strong binding affinity between RES and key senescence-associated proteins (SERPINE1: -8 kcal/mol; MMP2: -7.5 kcal/mol; IL-6: -7.1 kcal/mol). Conclusion: Resveratrol effectively inhibits alveolar epithelial cell senescence and ameliorates pulmonary fibrosis, likely by targeting key senescence-associated pathways (e.g., SERPINE1, MMP2, IL-6). This study provides a promising transdisciplinary strategy for anti-fibrotic drug discovery and highlights RES as a potential therapeutic candidate for PF.
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