Evidence map›Paper›PMID 42327275›Full record

ArticlebioRxiv : the preprint server for biology2026

Epigenetic de-repression of basal cell metaplasia in aging AT2 cells is a risk factor for idiopathic pulmonary fibrosis (IPF).

Stefano A Iantorno, Ying Wei, Kiana Garakani, Alexis N Brumwell, Tsung Che Ho, Marylene Toigo, Jaymin J Kathiriya, Asres Mitke, Vivianne Ding, Zea Borok and 5 more

Abstract readPreprint
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

15 authors.

Stefano A IantornoDepartment of Medicine, Division of Pulmonary, Critical Care, Allergy, and Sleep Medicine, University of California San Francisco, San Francisco, California.ORCID 0000-0001-5471-8913
Ying WeiDepartment of Medicine, Division of Pulmonary, Critical Care, Allergy, and Sleep Medicine, University of California San Francisco, San Francisco, California.
Kiana GarakaniDepartment of Medicine, Division of Pulmonary, Critical Care, Allergy, and Sleep Medicine, University of California San Francisco, San Francisco, California.ORCID 0000-0003-0739-4666
Alexis N BrumwellDepartment of Medicine, Division of Pulmonary, Critical Care, Allergy, and Sleep Medicine, University of California San Francisco, San Francisco, California.ORCID 0009-0006-8441-6354
Tsung Che HoDepartment of Medicine, Division of Pulmonary, Critical Care, Allergy, and Sleep Medicine, University of California San Francisco, San Francisco, California.
Marylene ToigoDepartment of Medicine, Division of Pulmonary, Critical Care, Allergy, and Sleep Medicine, University of California San Francisco, San Francisco, California.
Jaymin J KathiriyaDepartment of Stem Cell Biology and Regenerative Medicine, Icahn School of Medicine at Mount Sinai, New York, New York.
Asres MitkeDepartment of Medicine, Division of Pulmonary, Critical Care, Sleep Medicine, and Physiology, University of California San Diego, San Diego, California.
Vivianne DingDepartment of Surgery, Division of Thoracic Surgery, University of California San Francisco, San Francisco, California.
Zea BorokDepartment of Medicine, Division of Pulmonary, Critical Care, Sleep Medicine, and Physiology, University of California San Diego, San Diego, California.ORCID 0000-0001-8673-8177
Johannes KratzDepartment of Surgery, Division of Thoracic Surgery, University of California San Francisco, San Francisco, California.
Michael A MatthayDepartment of Medicine, Division of Pulmonary, Critical Care, Allergy, and Sleep Medicine, University of California San Francisco, San Francisco, California.
Paul J WoltersDepartment of Medicine, Division of Pulmonary, Critical Care, Allergy, and Sleep Medicine, University of California San Francisco, San Francisco, California.ORCID 0000-0002-3108-6164
Harold A ChapmanDepartment of Medicine, Division of Pulmonary, Critical Care, Allergy, and Sleep Medicine, University of California San Francisco, San Francisco, California.ORCID 0000-0002-5280-5527
Claude Jourdan Le SauxDepartment of Medicine, Division of Pulmonary, Critical Care, Allergy, and Sleep Medicine, University of California San Francisco, San Francisco, California.ORCID 0000-0002-6041-2870

Funding

MUTIDISCIPLINARY TRAINING PROGRAM IN LUNG DISEASEST32HL007185 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI David J Erle, LAURENCE HUANG · 1985 to 2026
$24.6M
Epithelial stem/progenitor cells as repair agents in diffuse alveolar damageU01HL134766 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI CHAPMAN, HAROLD A, KOTTON, DARRELL N. · 2016 to 2022
$8.1M
Program to promote lung regeneration and block fibrosisR35HL150767 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI CHAPMAN, HAROLD A · 2020 to 2025
$5.8M
Program to block age-related pulmonary fibrosis and restore lung regenerationR35HL183538 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI Harold A Chapman · 2026 to 2026
$1.1M
Epigenetic signatures driving metaplastic repair mechanisms in human alveolar type II cellsF32HL175915 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI Stefano Azelio Iantorno · 2024 to 2026
$265k
NHLBI NIH HHS F32 HL175915NHLBI NIH HHS R35 HL150767NHLBI NIH HHS R35 HL183538NHLBI NIH HHS T32 HL007185NHLBI NIH HHS U01 HL134766
6 · The paper itself

Abstract

Idiopathic pulmonary fibrosis (IPF) is a fatal, age-associated lung disease in which alveolar type II (AT2) cells lose regenerative capacity and can adopt aberrant basal-like fates that promote fibrosis. Using 3D organoid co-cultures with primary human fibroblasts, we find that healthy human AT2 cell trans-differentiation into KRT5+/KRT17+ basal cells increases progressively with age, while differentiation into RAGE+ AT1-like cells decreases. We identify a shared gene signature in AT2 cells at downstream targets of p63 characterized both by acquisition of bivalent, poised chromatin marks with age and increased accessibility in IPF, indicating epigenetic "priming" towards a basal cell lineage.

Identifiers

PMID42327275
PMCPMC13278176

What Socratic holds

Textmetadata
LicenceCC BY-NC
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.