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

Autotaxin NFAT1 PDGFR alpha positive mesenchymal cells fibrosis migration

Journal

American journal of physiology. Lung cellular and molecular physiology
ISSN: 1522-1504
Titre abrégé: Am J Physiol Lung Cell Mol Physiol
Pays: United States
ID NLM: 100901229

Informations de publication

Date de publication:
07 Nov 2023
Historique:
pubmed: 7 11 2023
medline: 7 11 2023
entrez: 7 11 2023
Statut: aheadofprint

Résumé

Idiopathic pulmonary fibrosis (IPF) is marked by unremitting matrix deposition and architectural distortion. Multiple pro-fibrotic 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 NFAT1 (nuclear factor of activated T cells 1) lies downstream of second messenger calcium signaling and has been recently shown to regulate key pro-fibrotic mediator autotaxin (ATX) in lung MCs. Herein, we investigate the role of NFAT1 in regulating fibroproliferative responses during the development of lung fibrosis.

Identifiants

DOI: 10.1152/ajplung.00045.2023 PMID: 37933452
pubmed: 37933452
doi: 10.1152/ajplung.00045.2023
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Subventions

Organisme : HHS | NIH | National Heart, Lung, and Blood Institute (NHLBI)
ID : HL118017
Organisme : HHS | NIH | National Heart, Lung, and Blood Institute (NHLBI)
ID : HL162171
Organisme : HHS | NIH | National Heart, Lung, and Blood Institute (NHLBI)
ID : HL094622
Organisme : Cystic Fibrosis Foundation (CFF)
ID : LAMA16XX0
Organisme : Campbell Foundation (The Campbell Foundation)
ID : Gift fund

Auteurs

Ragini Vittal (R)

Internal Medicine/PULM, Emory University, Ann Arbor, MI, United States.

Natalie M Walker (NM)

Division of Pulmonary and Critical Care, Department of Internal Medicine, University of Michigan-Ann Arbor, Ann Arbor, MI, United States.

A Patrick McLinden (AP)

Division of Pulmonary, Allergy, Critical Care, and Sleep Medicine, Department of Medicine, Emory University, Atlanta, GA, United States.

Russell R Braeuer (RR)

Division of Pulmonary and Critical Care, Department of Internal Medicine, University of Michigan-Ann Arbor, Ann Arbor, MI, United States.

Fang Ke (F)

Division of Pulmonary and Critical Care, Department of Internal Medicine, University of Michigan-Ann Arbor, Ann Arbor, MI, United States.

Fatemeh Fattahi (F)

Division of Pulmonary and Critical Care, Department of Internal Medicine, University of Michigan-Ann Arbor, Ann Arbor, MI, United States.

Michael P Combs (MP)

Division of Pulmonary and Critical Care, Department of Internal Medicine, University of Michigan-Ann Arbor, Ann Arbor, MI, United States.

Keizo Misumi (K)

Division of Pulmonary and Critical Care, Department of Internal Medicine, University of Michigan-Ann Arbor, Ann Arbor, MI, United States.

Yoshiro Aoki (Y)

Division of Pulmonary and Critical Care, Department of Internal Medicine, University of Michigan-Ann Arbor, Ann Arbor, MI, United States.

David S Wheeler (DS)

Division of Pulmonary and Critical Care, Department of Internal Medicine, University of Michigan-Ann Arbor, Ann Arbor, MI, United States.

Carol A Wilke (CA)

Department of Microbiology and Immunology, University of Michigan-Ann Arbor, Ann Arbor, MI, United States.

Steven K Huang (SK)

University of Michigan-Ann Arbor, Ann Arbor, MI, United States.

Bethany B Moore (BB)

Internal Medicine, University of Michigan-Ann Arbor, Ann Arbor, MI, United States.

Pengxiu Cao (P)

Key Laboaratory of Animal Physiology, Biochemistry and Molecular Biology of Hebei Province, College of Life Sciences, University of Michigan, Shijiazhuang, Hebei, China.

Vibha N Lama (VN)

Division of Pulmonary and Critical Care, Department of Internal Medicine, Emory University, Ann Arbor, MI, United States.

Classifications MeSH