Evidence map›Paper›PMID 41756935›Full record

ArticlebioRxiv : the preprint server for biology2026

IPF AT2 cells are stuck in transition and biophysically dysfunctional.

Andrey Krivoy, Daniel Sevilla-Sanchez, Ian T Stancil, Evgenia Dobrinskikh, S Zahra F Kiaei, Rachel Z Blumhagen, E Erin Smith, Ivana V Yang, Carlyne D Cool, Lior Atia and 1 more

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PubMed Full text at PMC Publisher
In one paragraph

Article in bioRxiv : the preprint server for biology, 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

11 authors.

Andrey KrivoyDepartment of Medicine, University of Colorado Anschutz; Aurora, 80045, USA.
Daniel Sevilla-SanchezIlse Katz Institute for Nanoscale Science and Technology, Ben-Gurion University of the Negev; Beer-Sheva, 84105, Israel.
Ian T StancilDepartment of Medicine, University of Colorado Anschutz; Aurora, 80045, USA.
Evgenia DobrinskikhDepartment of Medicine, University of Colorado Anschutz; Aurora, 80045, USA.
S Zahra F KiaeiDepartment of Medicine, University of Colorado Anschutz; Aurora, 80045, USA.
Rachel Z BlumhagenCenter for Genes, Environment and Health, National Jewish Health; Denver, 80206, USA.
E Erin SmithCancer Center Pathology Shared Resource, University of Colorado Anschutz; Aurora, 80045, USA.
Ivana V YangDepartment of Medicine, University of Colorado Anschutz; Aurora, 80045, USA.
Carlyne D CoolDepartment of Pathology, University of Colorado Anschutz; Aurora, 80045, USA.
Lior AtiaDepartment of Mechanical Engineering, Ben-Gurion University of the Negev; Beer-Sheva, 84105, Israel.
David A SchwartzDepartment of Medicine, University of Colorado Anschutz; Aurora, 80045, USA.

Funding

Targeting early events in MUC5B-driven lung injury and fibrosisP01HL162607 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI David Albert Schwartz · 2023 to 2026
$12.4M
MUC5B, a novel therapeutic target for Idiopathic Pulmonary Fibrosis (IPF)UH3HL123442 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI SCHWARTZ, DAVID ALBERT · 2016 to 2018
$4.8M
Molecular Determinants of Usual Interstitial Pneumonia (UIP)R01HL158668 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI David Albert Schwartz, Ivana V Yang · 2022 to 2026
$3.5M
MUC5B, a novel therapeutic target for Idiopathic Pulmonary Fibrosis (IPF)UH2HL123442 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI SCHWARTZ, DAVID ALBERT · 2014 to 2015
$3.0M
Genes and Transcripts that Interact with MUC5B in Pulmonary FibrosisR01HL149836 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI CLOUTHIER, DAVID E., SCHWARTZ, DAVID ALBERT · 2020 to 2023
$3.0M
Preclinical Pulmonary Fibrosis, an opportune rare disease cohortUG3HL151865 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI SCHWARTZ, DAVID ALBERT · 2020 to 2021
$1.7M
BLRD VA I01 BX005295NHLBI NIH HHS P01 HL162607NHLBI NIH HHS R01 HL149836NHLBI NIH HHS R01 HL158668NHLBI NIH HHS UG3 HL151865NHLBI NIH HHS UH2 HL123442NHLBI NIH HHS UH3 HL123442
6 · The paper itself

Abstract

Idiopathic Pulmonary Fibrosis (IPF) is an incurable disease with extensive molecular, cellular, and organ level dysfunction. A major gap in IPF research is the lack of understanding of how short-term cellular behavior causes long-term tissue remodeling. By optimizing lung slices from explanted human lungs, we discovered foci of migratory non-canonical alveolar type 2 (AT2) cells in regions of established lung fibrosis and found that these cells are trapped in states of cellular transition that are driven by persistent developmental repair programs. Consistent with these biophysical behaviors, pharmacological activation of β-catenin reproduced persistent migration, whereas YAP activation restrained it. We conclude that imbalanced developmental programs drive AT2 cell motility and lesion heterogeneity, providing a mechanistic link between short-term cellular dynamics and slowly progressive fibrosis of IPF.

Identifiers

PMID41756935
PMCPMC12934969

What Socratic holds

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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 Socratic graph.