Evidence map›Paper›PMID 42613079›Full record

ReviewEuropean respiratory review : an official journal of the European Respiratory Society2026

Murine models of pulmonary fibrosis: mechanisms, limitations and translational insights.

Karen F Lou, McKenzie M Fulcer, Mary J Lotesto, Jennifer M Davis, Tatiana P Ortiz Serrano, Ruihua Ma, Karen M Ridge

Abstract readReview
In one paragraph

Review in European respiratory review : an official journal of the European Respiratory Society, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors.

Karen F LouDivision of Pulmonary and Critical Care, Department of Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL, USA.
McKenzie M FulcerDivision of Pulmonary and Critical Care, Department of Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL, USA.
Mary J LotestoDivision of Pulmonary and Critical Care, Department of Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL, USA.
Jennifer M DavisDivision of Pulmonary and Critical Care, Department of Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL, USA.
Tatiana P Ortiz SerranoDivision of Pulmonary and Critical Care, Department of Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL, USA.
Ruihua MaDivision of Pulmonary and Critical Care, Department of Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL, USA ruihua.ma@northwestern.edu.
Karen M RidgeDivision of Pulmonary and Critical Care, Department of Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL, USA.

Funding

The Cell Phenotyping and Mouse CoreP01HL154998 · NHLBI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI KAREN M RIDGE · 2021 to 2026
$18.9M
Training Program In Lung SciencesT32HL076139 · NHLBI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI KAREN M RIDGE, Jacob I Sznajder · 2004 to 2026
$9.6M
Elucidating the Role of cGAS-STING in Lung Tissue Repair and RemodelingR01HL166807 · NHLBI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI KAREN M RIDGE · 2024 to 2026
$1.8M
NHLBI NIH HHS P01 HL154998NHLBI NIH HHS R01 HL166807NHLBI NIH HHS T32 HL076139
6 · The paper itself

Abstract

Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive, irreversible interstitial lung disease characterised by excessive collagen deposition, aberrant tissue remodelling, and impaired gas exchange, ultimately leading to respiratory failure and death. IPF carries a poor prognosis, with limited therapeutic options; currently approved treatments slow disease progression but do not reverse established fibrosis, and lung transplantation remains the only definitive therapy. Moreover, the prevalence and incidence of IPF continue to rise worldwide. These challenges underscore the urgent need to better understand the pathological mechanisms driving IPF, enabling the development of more effective therapeutic strategies. Robust and appropriate animal models are essential for investigating disease pathogenesis and therapeutic response. Although multiple murine models of pulmonary fibrosis are widely used, no single model fully recapitulates the clinical, pathological and temporal features of human IPF. In this review, we systematically summarise commonly used and new murine models of pulmonary fibrosis, emphasising induction methods, technical requirements, the time course of fibrosis development and persistence of fibrosis. Additionally, we highlight the advantages and limitations of each model, discuss how they inform mechanistic and translational studies, and provide practical guidance for selecting appropriate experimental systems based on specific scientific questions, with the goal of improving rigor and relevance in preclinical pulmonary fibrosis research.

Indexed as

Disease Models, AnimalIdiopathic Pulmonary FibrosisLungTranslational Research, BiomedicalAnimalsDisease ProgressionHumansMicePhenotypeSignal Transduction

Identifiers

PMID42613079
PMCPMC13482731

What OpenQuestion holds

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Read underepoch 390

Registered trials

None linked

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.