ReviewEuropean journal of medical research2025
Aging-associated interleukin-11 drives the molecular mechanism and targeted therapy of idiopathic pulmonary fibrosis.
Review in European journal of medical research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
5 citing papers in PubMed.
- Multi-omics insights into the mechanisms and prognosis of IPF.Genes and environment : the official journal of the Japanese Environmental Mutagen Society · 2026Review
- Idiopathic pulmonary fibrosis and interleukins: a bibliometric analysis [1999-2025].Journal of thoracic disease · 2026Article
- Synergistic senolytic-regenerative therapy significantly extends healthspan and lifespan.Journal of translational medicine · 2026Article
- Pulmonary Vascular Endothelial Cells in Lung Diseases: Mechanisms, Therapeutic Strategies, and Future Directions.Cell proliferation · 2026Review
- Identification of interleukin-11 as a comorbid risk factor for prostate cancer and Alzheimer's disease using integrated bioinformatics and machine learning.Frontiers in immunology · 2026Article
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
Idiopathic pulmonary fibrosis (IPF) is an unexplained interstitial lung disease in which senescence is a central risk factor. Senescent cells drive chronic inflammation and fibrosis by the secreting senescence-associated secretory phenotype (SASP). Interleukin-11 (IL-11), a core factor in the SASP, is significantly upregulated in IPF lung tissues.IL-11 promotes lung cellular senescence and chronic inflammation through the activation of the JAK2/STAT3 and MEK/ERK1/2 pathways. It also leads to extracellular matrix protein deposition by promoting fibroblast-myofibroblast transformation, epithelial mesenchymal transition and endothelial mesenchymal transition. Targeting IL-11 has antiaging and fibrotic effects. Nanoparticle delivery therapeutic regimens targeting IL-11 show potential in animal models of IPF, but evidence for their clinical application is lacking. Future studies should focus on the dynamic molecular regulatory mechanisms of IL-11 in IPF, as well as the development of targeted delivery systems and multitarget combined intervention therapeutic regimens. This review systematically analyzes the molecular mechanisms of IL-11 in IPF and provides new perspectives for the treatment of aging-associated pulmonary fibrosis.
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Registered trials
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