Evidence map›Paper›PMID 42685210›Full record

ArticleScience advances2026

Critical role for the TGF-β1/mTORC1 signaling axis in defining the transcriptional identity of CTHRC1

Jo-Anne Am Wilson, Rachel Walters, Greg Contento, Madeleine Rossanese, Delphine Guillotin, Alexander I Ward, Robert E Hynds, Mariam Jamal-Hanjani, Naftali Kaminski, Silvia Parolo and 2 more

Abstract read
In one paragraph

Article in Science advances, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Loss of lung mesenchymal identities in culture and a screening approach to identify restorative cues.American journal of physiology. Lung cellular and molecular physiology · 2025
    Article
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

12 authors.

Jo-Anne Am WilsonCentre for Inflammation and Tissue Repair, UCL Respiratory, University College London, London WC1E 6JF, UK.ORCID 0009-0007-6574-6507
Rachel WaltersCentre for Inflammation and Tissue Repair, UCL Respiratory, University College London, London WC1E 6JF, UK.ORCID 0000-0002-0743-9070
Greg ContentoCentre for Inflammation and Tissue Repair, UCL Respiratory, University College London, London WC1E 6JF, UK.
Madeleine RossaneseCentre for Inflammation and Tissue Repair, UCL Respiratory, University College London, London WC1E 6JF, UK.ORCID 0000-0002-0179-4354
Delphine GuillotinCentre for Inflammation and Tissue Repair, UCL Respiratory, University College London, London WC1E 6JF, UK.ORCID 0000-0002-2464-6848
Alexander I WardCentre for Inflammation and Tissue Repair, UCL Respiratory, University College London, London WC1E 6JF, UK.
Robert E HyndsEpithelial Cell Biology in ENT Research (EpiCENTR) Group, Developmental Biology and Cancer Department, Great Ormond Street UCL Institute of Child Health, University College London, London, UK.ORCID 0000-0002-2170-8791
Mariam Jamal-HanjaniEpithelial Cell Biology in ENT Research (EpiCENTR) Group, Developmental Biology and Cancer Department, Great Ormond Street UCL Institute of Child Health, University College London, London, UK.ORCID 0000-0003-1212-1259
Naftali KaminskiSection of Pulmonary, Critical Care and Sleep Medicine, Yale School of Medicine, New Haven, CT, USA.ORCID 0000-0001-5917-4601
Silvia ParoloFondazione The Microsoft Research - University of Trento Centre for Computational and Systems Biology (COSBI), Rovereto, Italy.ORCID 0000-0002-3671-5353
Manuela PlatéCentre for Inflammation and Tissue Repair, UCL Respiratory, University College London, London WC1E 6JF, UK.ORCID 0000-0002-9957-0681
Rachel C ChambersCentre for Inflammation and Tissue Repair, UCL Respiratory, University College London, London WC1E 6JF, UK.ORCID 0000-0003-1370-9417

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Fibrosis, marked by excess extracellular matrix (ECM) deposition, is the end stage of many diseases. Single-cell studies have highlighted the emergence of disease-specific fibroblast populations, including a high collagen-synthesizing

Indexed as

Extracellular Matrix ProteinsFibroblastsMechanistic Target of Rapamycin Complex 1Signal TransductionTranscription, GeneticTransforming Growth Factor beta1AnimalsGene Expression RegulationHumansIdiopathic Pulmonary FibrosisExtracellular Matrix ProteinsMechanistic Target of Rapamycin Complex 1Transforming Growth Factor beta1

Identifiers

PMID42685210
PMCPMC13537237

What OpenQuestion holds

Textmetadata
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.