ReviewExperimental and therapeutic medicine2025
Advances in understanding the role of interleukins in pulmonary fibrosis (Review).
Review in Experimental and therapeutic medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
4 citing papers in PubMed.
- Alpha-Lipoic Acid Attenuates Fibrotic and Inflammatory Dermal Remodelling in a Bleomycin-Induced Skin Model.Cell biochemistry and biophysics · 2026Article
- Protective Effects Assessment of Combined Extracts fromVeterinary sciences · 2026Article
- Interleukin-10 family cytokines: key regulators and novel therapeutic targets for respiratory diseases.Inflammopharmacology · 2025Review
- Emerging Concepts in Therapeutic Interventions for Idiopathic Pulmonary Fibrosis.Seminars in respiratory and critical care medicine · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pulmonary fibrosis (PF) is a progressive, irreversible disease characterized by heterogeneous interstitial lung tissue damage. It originates from persistent or repeated lung epithelial injury and leads to the activation and differentiation of fibroblasts into myofibroblasts. Interleukins (ILs) are a group of lymphokines crucial for immunomodulation that are implicated in the pathogenesis of PF. However, different types of ILs exert disparate effects on PF. In the present review, based on the effect on PF, ILs are classified into three categories: i) Promotors of PF; ii) inhibitors of PF; and iii) those that exert dual effects on PF. Several types of ILs can promote PF by provoking inflammation, initiating proliferation and transdifferentiation of epithelial cells, exacerbating lung injury, while other ILs can inhibit PF through suppressing expression of inflammatory factors, modulating the Th1/Th2 balance and autophagy. The present review summarizes the association of ILs and PF, focusing on the roles and mechanisms of ILs underlying PF.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.