ArticleMolecular and cellular biology2015
Orphan Nuclear Receptor Nur77 Inhibits Cardiac Hypertrophic Response to Beta-Adrenergic Stimulation.
Article in Molecular and cellular biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 45 citations in OpenAlex.
- PP2A-B56α is a key determinant of cardiac protein phosphorylation and functional responses to β-adrenergic signalling.Journal of molecular and cellular cardiology plus · 2025Article
- The universal role of adaptive transcription in health and disease.The FEBS journal · 2025Review
- Controversy and multiple roles of the solitary nucleus receptor Nur77 in disease and physiology.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Review
- Inhibiting endothelial cell Mst1 attenuates acute lung injury in mice.JCI insight · 2024Article
- Honokiol ameliorates angiotensin II-induced cardiac hypertrophy by promoting dissociation of the Nur77-LKB1 complex and activating the AMPK pathway.Journal of cellular and molecular medicine · 2024Article
- Epigenetic regulation of vascular smooth muscle cell phenotypic switch and neointimal formation by PRMT5.Cardiovascular research · 2023Article
- Transcriptomal Insights of Heart Failure from Normality to Recovery.Biomolecules · 2022Article
- Nur77 Deficiency Exacerbates Macrophage NLRP3 Inflammasome-Mediated Inflammation and Accelerates Atherosclerosis.Oxidative medicine and cellular longevity · 2022Article
- Nur77 Attenuates Inflammasome Activation by Inhibiting Caspase-1 Expression in Pulmonary Vascular Endothelial Cells.American journal of respiratory cell and molecular biology · 2021Article
- Untangling the Cooperative Role of Nuclear Receptors in Cardiovascular Physiology and Disease.International journal of molecular sciences · 2021Review
- Nur77 limits endothelial barrier disruption to LPS in the mouse lung.American journal of physiology. Lung cellular and molecular physiology · 2019Article
- Nuclear receptor subfamily 4 group A member 2 inhibits activation of ERK signaling and cell growth in response to β-adrenergic stimulation in adult rat cardiomyocytes.American journal of physiology. Cell physiology · 2019Article
- Long-term cardiovascular disorders in the STOX1 mouse model of preeclampsia.Scientific reports · 2019Article
- Article
- Endophilin A2 attenuates cardiac hypertrophy induced by isoproterenol through the activation of autophagy.American journal of translational research · 2019Article
- Transcriptional up-regulation of relaxin-3 by Nur77 attenuates β-adrenergic agonist-induced apoptosis in cardiomyocytes.The Journal of biological chemistry · 2018Article
- Gene expression analysis to identify mechanisms underlying heart failure susceptibility in mice and humans.Basic research in cardiology · 2018Article
- Effects of 4(1H)-quinolinone derivative, a novel non-nucleotide allosteric purinergic P2YScientific reports · 2017Article
- Cardiac nuclear receptors: architects of mitochondrial structure and function.The Journal of clinical investigation · 2017Review
- Glucose regulates the intrinsic inflammatory response of the heart to surgically induced hypothermic ischemic arrest and reperfusion.Physiological genomics · 2017Article
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 2 countries.
Funding
Abstract
The orphan nuclear receptor Nur77 plays critical roles in cardiovascular diseases, and its expression is markedly induced in the heart after beta-adrenergic receptor (β-AR) activation. However, the functional significance of Nur77 in β-AR signaling in the heart remains unclear. By using Northern blot, Western blot, and immunofluorescent staining assays, we showed that Nur77 expression was markedly upregulated in cardiomyocytes in response to multiple hypertrophic stimuli, including isoproterenol (ISO), phenylephrine (PE), and endothelin-1 (ET-1). In a time- and dose-dependent manner, ISO increases Nur77 expression in the nuclei of cardiomyocytes. Overexpression of Nur77 markedly inhibited ISO-induced cardiac hypertrophy by inducing nuclear translocation of Nur77 in cardiomyocytes. Furthermore, cardiac overexpression of Nur77 by intramyocardial injection of Ad-Nur77 substantially inhibited cardiac hypertrophy and ameliorated cardiac dysfunction after chronic infusion of ISO in mice. Mechanistically, we demonstrated that Nur77 functionally interacts with NFATc3 and GATA4 and inhibits their transcriptional activities, which are critical for the development of cardiac hypertrophy. These results demonstrate for the first time that Nur77 is a novel negative regulator for the β-AR-induced cardiac hypertrophy through inhibiting the NFATc3 and GATA4 transcriptional pathways. Targeting Nur77 may represent a potentially novel therapeutic strategy for preventing cardiac hypertrophy and heart failure.
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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 OpenQuestion graph.