Evidence map›Paper›PMID 35805179›Full record

ReviewCells2022

Regeneration or Repair? The Role of Alveolar Epithelial Cells in the Pathogenesis of Idiopathic Pulmonary Fibrosis (IPF).

Paola Confalonieri, Maria Concetta Volpe, Justin Jacob, Serena Maiocchi, Francesco Salton, Barbara Ruaro, Marco Confalonieri, Luca Braga

Open access · goldAbstract readReview
In one paragraph

Review in Cells, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 102 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
102citing papers in PubMed, 1 pooled it
19.9field-weighted citation impact, top 1% of its field
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

102 citing papers in PubMed, 1 synthesis or guideline pooled it, 140 citations in OpenAlex.

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  18. RIPK3 Orchestrates Scar-Associated Macrophage Dysfunction to Drive Pulmonary Fibrosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
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42 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

8 authors at 2 institutions in 1 country.

Paola ConfalonieriPulmonology Department, Cattinara Hospital, University of Trieste, 34127 Trieste, Italy.
Maria Concetta VolpeFunctional Cell Biology Group, International Centre for Genetic Engineering and Biotechnology (ICGEB), 34149 Trieste, Italy.
Justin JacobFunctional Cell Biology Group, International Centre for Genetic Engineering and Biotechnology (ICGEB), 34149 Trieste, Italy.ORCID 0000-0003-0883-0706
Serena MaiocchiFunctional Cell Biology Group, International Centre for Genetic Engineering and Biotechnology (ICGEB), 34149 Trieste, Italy.ORCID 0000-0002-5886-5731
Francesco SaltonPulmonology Department, Cattinara Hospital, University of Trieste, 34127 Trieste, Italy.ORCID 0000-0002-0864-9766
Barbara RuaroPulmonology Department, Cattinara Hospital, University of Trieste, 34127 Trieste, Italy.ORCID 0000-0001-8990-859X
Marco ConfalonieriPulmonology Department, Cattinara Hospital, University of Trieste, 34127 Trieste, Italy.ORCID 0000-0002-4791-768X
Luca BragaFunctional Cell Biology Group, International Centre for Genetic Engineering and Biotechnology (ICGEB), 34149 Trieste, Italy.ORCID 0000-0002-9827-6755
University of Trieste · ITInternational Centre for Genetic Engineering and Biotechnology · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive interstitial lung disease (ILD) with unknown etiology in which gradual fibrotic scarring of the lungs leads to usual interstitial pneumonia (UIP) and, ultimately, to death. IPF affects three million people worldwide, and the only currently available treatments include the antifibrotic drugs nintedanib and pirfenidone, which effectively reduce fibrosis progression are, unfortunately, not effective in curing the disease. In recent years, the paradigm of IPF pathogenesis has shifted from a fibroblast-driven disease to an epithelium-driven disease, wherein, upon recurrent microinjuries, dysfunctional alveolar type II epithelial cells (ATII) are not only unable to sustain physiological lung regeneration but also promote aberrant epithelial-mesenchymal crosstalk. This creates a drift towards fibrosis rather than regeneration. In the context of this review article, we discuss the most relevant mechanisms involved in IPF pathogenesis with a specific focus on the role of dysfunctional ATII cells in promoting disease progression. In particular, we summarize the main causes of ATII cell dysfunction, such as aging, environmental factors, and genetic determinants. Next, we describe the known mechanisms of physiological lung regeneration by drawing a parallel between embryonic lung development and the known pathways involved in ATII-driven alveolar re-epithelization after injury. Finally, we review the most relevant interventional clinical trials performed in the last 20 years with the aim of underlining the urgency of developing new therapies against IPF that are not only aimed at reducing disease progression by hampering ECM deposition but also boost the physiological processes of ATII-driven alveolar regeneration.

Indexed as

Idiopathic Pulmonary FibrosisAlveolar Epithelial CellsDisease ProgressionFibrosisHumansLungATII cellsIPFregenerationsenescence

Identifiers

PMID35805179
PMCPMC9266271
OpenAlexW4283758424

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.