Evidence map›Paper›PMID 37933452›Full record

ArticleAmerican journal of physiology. Lung cellular and molecular physiology2024

Genetic deficiency of the transcription factor NFAT1 confers protection against fibrogenic responses independent of immune influx.

Ragini Vittal, Natalie M Walker, A Patrick McLinden, Russell R Braeuer, Fang Ke, Fatemeh Fattahi, Michael P Combs, Keizo Misumi, Yoshiro Aoki, David S Wheeler and 5 more

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in American journal of physiology. Lung cellular and molecular physiology, 2024. 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
0.2field-weighted citation impact, top 40% 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

1 citing paper in PubMed, 1 citations in OpenAlex.

  1. 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

15 authors at 2 institutions in 1 country.

Ragini VittalDivision of Pulmonary, Allergy, Critical Care, and Sleep Medicine, Department of Medicine, School of Medicine, Emory University, Atlanta, Georgia, United States.
Natalie M WalkerDivision of Pulmonary & Critical Care Medicine, Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan, United States.
A Patrick McLindenDivision of Pulmonary, Allergy, Critical Care, and Sleep Medicine, Department of Medicine, School of Medicine, Emory University, Atlanta, Georgia, United States.
Russell R BraeuerDivision of Pulmonary & Critical Care Medicine, Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan, United States.
Fang KeDivision of Pulmonary & Critical Care Medicine, Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan, United States.
Fatemeh FattahiDivision of Pulmonary & Critical Care Medicine, Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan, United States.
Michael P CombsDivision of Pulmonary & Critical Care Medicine, Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan, United States.
Keizo MisumiDivision of Pulmonary & Critical Care Medicine, Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan, United States.
Yoshiro AokiDivision of Pulmonary & Critical Care Medicine, Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan, United States.ORCID 0000-0003-1591-5345
David S WheelerDivision of Pulmonary & Critical Care Medicine, Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan, United States.
Carol A WilkeDepartment of Microbiology & Immunology, University of Michigan, Ann Arbor, Michigan, United States.
Steven K HuangDivision of Pulmonary & Critical Care Medicine, Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan, United States.ORCID 0000-0002-2090-6331
Bethany B MooreDepartment of Microbiology & Immunology, University of Michigan, Ann Arbor, Michigan, United States.ORCID 0000-0003-3051-745X
Pengxiu CaoDivision of Pulmonary & Critical Care Medicine, Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan, United States.ORCID 0000-0002-5900-5645
Vibha N LamaDivision of Pulmonary, Allergy, Critical Care, and Sleep Medicine, Department of Medicine, School of Medicine, Emory University, Atlanta, Georgia, United States.ORCID 0000-0002-5157-777X
University of Michigan · USEmory University · US

Funding

Translational Dysregulation Driving Mesenchymal Cell Fibrogenic Transformation and Chronic Lung Allograft DysfunctionR01HL094622 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI LAMA, VIBHA N · 2009 to 2023
$5.9M
The Role of KCNMB1 and the Large Conductance Potassium (BK) Channel in Myofibroblast Differentiation and Pulmonary FibrosisR01HL127203 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI HUANG, STEVEN K · 2015 to 2024
$4.4M
Heterogeneity and Regulation of the DNA Methylome in IPF Mesenchymal CellsR01HL162963 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI STEVEN K HUANG · 2023 to 2026
$2.7M
Pathogenesis of Restrictive Allograft Syndrome Post-Lung TransplantationR01HL162171 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI LAMA, VIBHA N · 2022 to 2025
$2.7M
Autotaxin Lysophophatidic acid pathway in bronchiolitis obliterans post-lung tranR01HL118017 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI LAMA, VIBHA N · 2014 to 2017
$2.0M
NHLBI NIH HHS R01 HL094622NHLBI NIH HHS R01 HL118017NHLBI NIH HHS R01 HL127203NHLBI NIH HHS R01 HL162171NHLBI NIH HHS R01 HL162963
6 · The paper itself

Abstract

Idiopathic pulmonary fibrosis (IPF) is marked by unremitting matrix deposition and architectural distortion. Multiple profibrotic pathways contribute to the persistent activation of mesenchymal cells (MCs) in fibrosis, highlighting the need to identify and target common signaling pathways. The transcription factor nuclear factor of activated T cells 1 (NFAT1) lies downstream of second messenger calcium signaling and has been recently shown to regulate key profibrotic mediator autotaxin (ATX) in lung MCs. Herein, we investigate the role of NFAT1 in regulating fibroproliferative responses during the development of lung fibrosis.

Indexed as

Idiopathic Pulmonary FibrosisLungAnimalsBleomycinCell DifferentiationFibroblastsHumansMiceMice, Inbred C57BLNFATC Transcription FactorsSignal TransductionBleomycinNFATC2 protein, humanNfatc2 protein, mouseNFATC Transcription FactorsautotaxinfibrosismigrationNFAT1PDGFRα+ mesenchymal cells

Identifiers

PMID37933452
PMCPMC11279780
OpenAlexW4388462564

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.