Key Functions and Therapeutic Prospects of Nur77 in Inflammation Related Lung Diseases
Open accessAbstract
The transcription factor Nur77 belongs to the NR4A subfamily of nuclear hormone receptors. It features an atypical ligand-binding site that precludes canonical ligand binding, leading to the designation orphan nuclear receptor. However, recent studies show that small molecules can interact with the receptor and modulate its activity by inducing a conformational change in the Nur77 ligand-binding site. Nur77 expression and activation are rapidly induced by various physiological and pathologic stimuli. Once expressed, Nur77 initiates transcriptional activity and modulates expression of its target genes. Both in vitro and in vivo evidence shows that Nur77 dampens the immune response to proinflammatory stimuli, such as tumor necrosis factor-α, Toll-like receptor ligands, and oxidized lipids, primarily by suppressing NF-κB signaling. Although studies focusing on Nur77's role in lung pathophysiology are currently incomplete, available data support its involvement in the pathogenesis of lung diseases, including asthma, acute lung injury, and pulmonary fibrosis, and thus suggest a therapeutic potential for Nur77 activation in these diseases. This review addresses the mechanisms that control Nur77 as well as its known roles in inflammation-related lung diseases. Evidence regarding the therapeutic potential of Nur77-targeting molecules will also be presented. Although current knowledge is limited, additional research followed by clinical studies may firmly identify Nur77 as a pharmacologic target for inflammation-related lung diseases.
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Transcriptome revealed decreased expression of NR4A nuclear receptors (NR4A1, NR4A2, NR4A3) in hEDS/HSD cells.
“As further evidence of unbalanced inflammatory responses in patients’ cells, transcriptome revealed a decreased expression of the NR4A nuclear receptors (NR4A1, NR4A2, NR4A3), which act as transcriptional regulators of inflammatory responses mediated by NF-kB signaling [159,160,161].”
From Cellular and Molecular Mechanisms in the Pathogenesis of Classical, Vascular, and Hypermobile Ehlers‒Danlos Syndromes (2019) · cites this paper as [161]
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- Authors
- Banno, A., Lakshmi, S. P., Reddy, A. T., Kim, S. C., & Reddy, R. C.
- Affiliations
- University of Pittsburgh (US)
- Corresponding author
- Reddy, Raju C.
- Venue
- The American Journal of Pathology
- Publisher
- Elsevier BV
- Published
- 2019-03
- Volume
- 189
- Issue
- 3
- Pages
- 482-491
- ISSN
- 0002-9440 (ISSN-L)
- PMC
- PMC6458520
- OpenAlex
- W2900150319
- Cited by
- 53
- References
- 75
- Citations by year
- 2026: 7 · 2025: 5 · 2024: 11 · 2023: 9 · 2022: 5 · 2021: 7 · 2020: 7 · 2019: 2
- FWCI
- 0.52
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- American Journal Of Pathology (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (AI125338, HL137842)
- U.S. Department of Veterans Affairs
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nuclear Receptors and Signaling
- Health Sciences › Medicine › Geriatrics and Gerontology › Sirtuins and Resveratrol in Medicine
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics, phytochemicals, and oxidative stress
- Keywords
- Nur77, orphan nuclear receptor, NF-κB signaling, inflammation, lung disease, asthma, acute lung injury, pulmonary fibrosis, Toll-like receptor ligands, TNF-α, oxidized lipids, transcriptional regulation, therapeutic target
- MeSH terms
- Animals, Humans, Inflammation, Lung, Lung Diseases, Transcription, Genetic, Tumor Necrosis Factor-alpha, Signal Transduction, NF-kappa B, Toll-Like Receptors, Nuclear Receptor Subfamily 4, Group A, Member 1
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