ArticleCirculation2020
Cytokine mRNA Degradation in Cardiomyocytes Restrains Sterile Inflammation in Pressure-Overloaded Hearts.
Article in Circulation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 23 papers.
What it found
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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.
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Who cites it
23 citing papers in PubMed, 33 citations in OpenAlex.
- Decoding Regnase-1's role in skin inflammation: potential therapeutic implication for dermatological disorders.Journal of advanced research · 2026Review
- The Regnase pathway: a core axis in immune regulation and inflammatory disease.Frontiers in immunology · 2026Review
- The role of the bidirectional regulatory network between immune cells and stromal cells in cardiac repair and fibrosis following myocardial infarction.Frontiers in immunology · 2026Review
- ZC3H12A: A Critical Mediator of Inflammation, Tumor Immunotherapy, and Metabolic-Immune Crosstalk-Implications for Disease Treatment.Biomolecules · 2025Review
- Cardiomyocytes regulate Inflammation in the failing heart.American journal of physiology. Heart and circulatory physiology · 2025Article
- A Comprehensive Review: Unraveling the Role of Inflammation in the Etiology of Heart Failure.Heart failure reviews · 2025Review
- Mechanisms of mitochondrial damage-associated molecular patterns associated with inflammatory response in cardiovascular diseases.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Review
- Crosstalk between myocardial autophagy and sterile inflammation in the development of heart failure.Autophagy reports · 2024Review
- Review
- Lysophosphatidylserine induces necrosis in pressure overloaded male mouse hearts via G protein coupled receptor 34.Nature communications · 2023Article
- Pathophysiological Effects of Various Interleukins on Primary Cell Types in Common Heart Disease.International journal of molecular sciences · 2023Review
- iNOS aggravates pressure overload-induced cardiac dysfunction via activation of the cytosolic-mtDNA-mediated cGAS-STING pathway.Theranostics · 2023Article
- Effect of systemic corticosteroid therapy for acute heart failure patients with elevated C-reactive protein.ESC heart failure · 2022Article
- TRAF2, an Innate Immune Sensor, Reciprocally Regulates Mitophagy and Inflammation to Maintain Cardiac Myocyte Homeostasis.JACC. Basic to translational science · 2022Article
- Rubicon-regulated beta-1 adrenergic receptor recycling protects the heart from pressure overload.Scientific reports · 2022Article
- NF-κB activation in cardiac fibroblasts results in the recruitment of inflammatory Ly6CScience signaling · 2021Article
- The trans-omics landscape of COVID-19.Nature communications · 2021Article
- Article
- The contribution of the cardiomyocyte to tissue inflammation in cardiomyopathies.Current opinion in physiology · 2021Article
- Targeted Therapy in Cardiovascular Disease: A Precision Therapy Era.Frontiers in pharmacology · 2021Review
Corrections and comments
- Erratum issued
Authors and funding
12 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundProinflammatory cytokines play an important role in the pathogenesis of heart failure. The mechanisms responsible for maintaining sterile inflammation within failing hearts remain poorly defined. Although transcriptional control is important for proinflammatory cytokine gene expression, the stability of mRNA also contributes to the kinetics of immune responses. Regnase-1 is an RNase involved in the degradation of a set of proinflammatory cytokine mRNAs in immune cells. The role of Regnase-1 in nonimmune cells such as cardiomyocytes remains to be elucidated.
methodsTo examine the role of proinflammatory cytokine degradation by Regnase-1 in cardiomyocytes, cardiomyocyte-specific Regnase-1-deficient mice were generated. The mice were subjected to pressure overload by means of transverse aortic constriction to induce heart failure. Cardiac remodeling was assessed by echocardiography as well as histological and molecular analyses 4 weeks after operation. Inflammatory cell infiltration was examined by immunostaining. Interleukin-6 signaling was inhibited by administration with its receptor antibody. Overexpression of Regnase-1 in the heart was performed by adeno-associated viral vector-mediated gene transfer.
resultsCardiomyocyte-specific Regnase-1-deficient mice showed no cardiac phenotypes under baseline conditions, but exhibited severe inflammation and dilated cardiomyopathy after 4 weeks of pressure overload compared with control littermates. Four weeks after transverse aortic constriction, the
conclusionsThe degradation of cytokine mRNA by Regnase-1 in cardiomyocytes plays an important role in restraining sterile inflammation in failing hearts and the Regnase-1-mediated pathway might be a therapeutic target to treat patients with 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.