ReviewFrontiers in pharmacology2025
Current advancements in the mechanisms and animal models of acute exacerbation of pulmonary fibrosis: a systematic review.
Review 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 5 papers.
What it found
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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
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.
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Who cites it
5 citing papers in PubMed.
- Can the Prognostic Nutritional Index Be a Predictor of Acute Exacerbation of Idiopathic Pulmonary Fibrosis?Biomedicines · 2026Article
- Broad-Spectrum Protective Effects of Lyophilized FE002-Lu Lung Fibroblast Conditioned Medium Against Acute and Chronic Pulmonary Injury in Wistar Rats.Biomedicines · 2026Article
- Plasma SH Concentrations and Mortality in Patients with Newly Diagnosed Idiopathic Pulmonary Fibrosis.Antioxidants (Basel, Switzerland) · 2026Article
- Regulated Cell Death in Idiopathic Pulmonary Fibrosis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Review
- Nanocarrier-Enabled siRNA Therapy for Pulmonary Fibrosis: Pharmacological Rationale, Delivery Barriers, and Translational Opportunities.International journal of nanomedicine · 2026Review
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Characterized by sudden onset, accelerated disease progression, and high mortality rates, acute exacerbation (AE) represents the most critical clinical challenge faced by patients with idiopathic pulmonary fibrosis (IPF). The absence of standardized animal models that recapitulate human disease phenotypes remains a significant impediment to the study of AE-IPF. In this work, we conducted a systematic review of experimental protocols for acute exacerbation of pulmonary fibrosis (AE-PF) over the past 20 years relating to aspects such as animal species, drugs, drug doses, drug administration routes, and model characteristics, and summarized research progress on the mechanism underlying this condition. Statistical analysis revealed that bleomycin combined with lipopolysaccharide represents the predominant experimental paradigm for AE-PF, accounting for 26.3% (5/19) of all AE-PF models. Our analysis further showed that the major mechanisms involved in AE-IPF are inflammation, immune imbalance, oxidative stress, endoplasmic reticulum (ER) stress, and apoptosis of alveolar epithelial cells.
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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 Socratic graph.