ArticleCellular and molecular life sciences : CMLS2024
The orphan nuclear receptor Nr4a1 contributes to interstitial cardiac fibrosis via modulation of cardiac fibroblast and macrophage phenotype.
Article in Cellular and molecular life sciences : CMLS, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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The trial behind it
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Who cites it
8 citing papers in PubMed.
- Neutrophil depletion exacerbatesFood and waterborne parasitology · 2026Article
- Targeting NR4A1 (Nur77) in Macrophage Polarization: Molecular Mechanisms and Translational Prospects for Cardiac Repair After Myocardial Infarction.International journal of molecular sciences · 2026Review
- Neurokinin-1 receptor activation protects against cardiac fibrosis, inflammation and diastolic dysfunction in type 2 diabetic mice.British journal of pharmacology · 2026Article
- SAMHD1 promotes cardiac repair post myocardial infarction by targeting NR4a1 to regulate macrophage metabolic reprogramming.Journal of advanced research · 2026Article
- Targeting Complement Component 1q Ameliorates Diabetic Endothelial Inflammation Via Orphan Nuclear Receptor 4a1-Dependent Suppression of Nuclear Factor κB Signaling.Journal of the American Heart Association · 2026Article
- NR4A1 Regulates Glycolysis in M1 Macrophages via the Wnt/β-Catenin Pathway to Affect Sepsis-Induced Myocardial Injury.Journal of inflammation research · 2026Article
- Review
- Identification of glycolysis-related gene signatures for prognosis and therapeutic targeting in idiopathic pulmonary fibrosis.Frontiers in pharmacology · 2025Article
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The orphan nuclear receptor Nr4a1 has complex biological functions and has been implicated in numerous diseases, including cardiovascular disease. While protective in atherosclerosis and myocardial ischemia, Nr4a1 has been shown to cause cardiac fibrosis in non-ischemic adverse remodeling of the heart. However, mechanisms underlying these actions are still poorly understood. Accordingly, we sought to: (1) understand the contribution of Nr4a1 to the inflammatory environment including macrophage phenotype; and (2) determine the contribution of Nr4a1 to cardiac fibroblast phenotype in the fibrotic heart. Wild type and Nr4a1
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Registered trials
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.