Evidence map›Paper›PMID 37882943›Full record

ReviewDrugs2023

Current and Future Treatment Landscape for Idiopathic Pulmonary Fibrosis.

Francesco Bonella, Paolo Spagnolo, Chris Ryerson

Abstract readReview
In one paragraph

Review in Drugs, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 109 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
109citing papers in PubMed, 4 pooled it
–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

109 citing papers in PubMed, 4 syntheses or guidelines pooled it.

  1. Pooled it
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  5. Trial
  6. Article
  7. Folate metabolism-related gene signature reveals prognostic and immunological characteristics in idiopathic pulmonary fibrosis.Sarcoidosis, vasculitis, and diffuse lung diseases : official journal of WASOG · 2026
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49 more citing papers are in PubMed but not listed here.

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

3 authors.

Francesco BonellaPneumology Department, Center for Interstitial and Rare Lung Diseases, Ruhrlandklinik University Hospital, University of Duisburg Essen, Essen, Germany. francesco.bonella@rlk.uk-essen.de.ORCID http://orcid.org/0000-0001-7579-9767
Paolo SpagnoloCardiac, Thoracic and Vascular, Sciences and Public Health, University of Padova School of Medicine and Surgery, Padua, Italy.
Chris RyersonDepartment of Medicine, The University of British Columbia, Vancouver, BC, Canada.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Idiopathic pulmonary fibrosis (IPF) remains a disease with poor survival. The pathogenesis is complex and encompasses multiple molecular pathways. The first-generation antifibrotics pirfenidone and nintedanib, approved more than 10 years ago, have been shown to reduce the rate of progression, increase the length of life for patients with IPF, and work for other fibrotic lung diseases. In the last two decades, most clinical trials on IPF have failed to meet the primary endpoint and an urgent unmet need remains to identify agents or treatment strategies that can stop disease progression. The pharmacotherapeutic landscape for IPF is moving forward with a number of new drugs currently in clinical development, mostly in phase I and II trials, while only a few phase III trials are running. Since our understanding of IPF pathogenesis is still limited, we should keep focusing our efforts to deeper understand the mechanisms underlying this complex disease and their reflection on clinical phenotypes. This review discusses the key pathogenetic concepts for the development of new antifibrotic agents, presents the newest data on approved therapies, and summarizes new compounds currently in clinical development. Finally, future directions in antifibrotics development are discussed.

Indexed as

Idiopathic Pulmonary FibrosisHumansPhenotypePyridonesPyridones

Identifiers

PMID37882943
PMCPMC10693523

What OpenQuestion holds

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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.