ReviewBiomolecules2015
Molecular Interactions between NR4A Orphan Nuclear Receptors and NF-κB Are Required for Appropriate Inflammatory Responses and Immune Cell Homeostasis.
Review in Biomolecules, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
What it found
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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.
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.
Who cites it
48 citing papers in PubMed, 77 citations in OpenAlex.
- The Footprints of Poly-Autoimmunity: Evidence for Common Biological Factors Involved in Multiple Sclerosis and Hashimoto's Thyroiditis.Frontiers in immunology · 2018Trial
- PROTAC-mediated targeting of IKKβ and NR4A1 for AML therapy.Oncogene · 2026Article
- Pre-existing antibodies predict protection while mucosal inflammation correlates with symptomaticmedRxiv : the preprint server for health sciences · 2026Article
- Differential Expression Profiles of Orphan Nuclear Receptors (NR4A) and N-myc Downstream-Regulated Gene Family (NDRG) in Patients with Inflammatory Bowel Disease.International journal of molecular sciences · 2026Article
- Childhood adversity and increased cytokine release from peripheral mononuclear cells of CHD patients - a pilot study.BMC cardiovascular disorders · 2026Article
- Article
- Integrative multi-omics analysis reveals gut-skin axis mechanisms and novel therapeutic targetmSystems · 2026Article
- Oxytocin Modulates Microglial IL-17-Linked Inflammatory Pathways Through the IL-6/COX-2.Life (Basel, Switzerland) · 2026Article
- FABP5 regulates an immunosuppressive microenvironment in hepatocellular carcinoma through the NF-κB/PD-L1 axis.PloS one · 2026Article
- Identification and Analysis of Potential Biomarkers Associated with Neutrophil Extracellular Traps in Cervicitis.Biochemical genetics · 2025Article
- Regulation ofInternational journal of molecular sciences · 2025Review
- OTUB2/NR4A1 restrains the development of preeclampsia by suppressing macrophage M1 polarization.Communications biology · 2025Article
- Review
- A narrative review on bridging the gap between periodontitis and cardiovascular disease: exploring the cellular and molecular mechanisms of periodontitis-driven atherosclerosis.Molecular biology reports · 2025Review
- Target Role of Monocytes as Key Cells of Innate Immunity in Rheumatoid Arthritis.Diseases (Basel, Switzerland) · 2024Review
- Article
- Role of nutraceutical against exposure to pesticide residues: power of bioactive compounds.Frontiers in nutrition · 2024Review
- IGF2-NR4A2 Signaling Regulates Macrophage Subtypes to Attenuate Liver Cirrhosis.Journal of clinical and translational hepatology · 2023Article
- Effects of miR-33 Deficiency on Metabolic and Cardiovascular Diseases: Implications for Therapeutic Intervention.International journal of molecular sciences · 2023Review
- Nur77 and PPARγ regulate transcription and polarization in distinct subsets of M2-like reparative macrophages during regenerative inflammation.Frontiers in immunology · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Appropriate innate and adaptive immune responses are essential for protection and resolution against chemical, physical or biological insults. Immune cell polarization is fundamental in orchestrating distinct phases of inflammation, specifically acute phase responses followed by resolution and tissue repair. Dysregulation of immune cell and inflammatory responses is a hallmark of multiple diseases encompassing atherosclerosis, rheumatoid arthritis, psoriasis and metabolic syndromes. A master transcriptional mediator of diverse inflammatory signaling and immune cell function is NF-κB, and altered control of this key regulator can lead to an effective switch from acute to chronic inflammatory responses. Members of the nuclear receptor (NR) superfamily of ligand-dependent transcription factors crosstalk with NF-κB to regulate immune cell function(s). Within the NR superfamily the NR4A1-3 orphan receptors have emerged as important regulators of immune cell polarization and NF-κB signaling. NR4A receptors modulate NF-κB activity in a dynamic fashion, either repressing or enhancing target gene expression leading to altered inflammatory outcome. Here we will discuss the pivotal role NR4A's receptors play in orchestrating immune cell homeostasis through molecular crosstalk with NF-κB. Specifically, we will examine such NR4A/NF-κB interactions within the context of distinct cell phenotypes, including monocyte, macrophage, T cells, endothelial, and mesenchymal cells, which play a role in inflammation-associated disease. Finally, we review the therapeutic potential of altering NR4A/NF-κB interactions to limit hyper-inflammatory responses in vivo.
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What OpenQuestion holds
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 OpenQuestion graph.