ArticleMediators of inflammation2012
High-mobility group box 1 induces calcineurin-mediated cell hypertrophy in neonatal rat ventricular myocytes.
Article in Mediators of inflammation, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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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.
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Who cites it
19 citing papers in PubMed, 30 citations in OpenAlex.
- Long noncoding RNA AK144717 exacerbates pathological cardiac hypertrophy through modulating the cellular distribution of HMGB1 and subsequent DNA damage response.Cellular and molecular life sciences : CMLS · 2024Article
- Role of High Mobility Group Box 1 in Cardiovascular Diseases.Inflammation · 2022Review
- Recombinant high‑mobility group box 1 induces cardiomyocyte hypertrophy by regulating the 14‑3‑3η, PI3K and nuclear factor of activated T cells signaling pathways.Molecular medicine reports · 2021Article
- Increased Death of Peripheral Blood Mononuclear Cells after TLR4 Inhibition in Sepsis Is Not via TNF/TNF Receptor-Mediated Apoptotic Pathway.Mediators of inflammation · 2021Article
- Novel Therapeutic Effects of Pterosin B on Ang II-Induced Cardiomyocyte Hypertrophy.Molecules (Basel, Switzerland) · 2020Article
- HMGB1 enhances mechanical stress-induced cardiomyocyte hypertrophy in vitro via the RAGE/ERK1/2 signaling pathway.International journal of molecular medicine · 2019Article
- Cardiac Nuclear High-Mobility Group Box 1 Ameliorates Pathological Cardiac Hypertrophy by Inhibiting DNA Damage Response.JACC. Basic to translational science · 2019Article
- The Janus face of HMGB1 in heart disease: a necessary update.Cellular and molecular life sciences : CMLS · 2019Review
- Simvastatin Protects Heart from Pressure Overload Injury by Inhibiting Excessive Autophagy.International journal of medical sciences · 2018Article
- A Periodontal pathogen Porphyromonas gingivalis deteriorates Isoproterenol-Induced myocardial remodeling in mice.Hypertension research : official journal of the Japanese Society of Hypertension · 2017Article
- Extracellular high-mobility group box 1 mediates pressure overload-induced cardiac hypertrophy and heart failure.Journal of cellular and molecular medicine · 2016Article
- HMGB1-RAGE Axis Makes No Contribution to Cardiac Remodeling Induced by Pressure-Overload.PloS one · 2016Article
- Serum apelin is associated with left ventricular hypertrophy in untreated hypertension patients.Journal of translational medicine · 2015Article
- Protective effect of olmesartan against cardiac ischemia/reperfusion injury in spontaneously hypertensive rats.Experimental and therapeutic medicine · 2015Article
- The association between BMP4 gene polymorphism and its serum level with the incidence of LVH in hypertensive patients.Journal of translational medicine · 2015Article
- HMGB1 in health and disease.Molecular aspects of medicine · 2014Review
- Article
- Serum osteopontin, but not OPN gene polymorphism, is associated with LVH in essential hypertensive patients.Journal of molecular medicine (Berlin, Germany) · 2014Article
- Innate immunity and cardiomyocytes in ischemic heart disease.Life sciences · 2014Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cardiac hypertrophy is an independent predictor of cardiovascular morbidity and mortality. In recent years, evidences suggest that high-mobility group box 1 (HMGB1) protein, an inflammatory cytokine, participates in cardiac remodeling; however, the involvement of HMGB1 in the pathogenesis of cardiac hypertrophy remains unknown. The aim of this study was to investigate whether HMGB1 is sufficient to induce cardiomyocyte hypertrophy and to identify the possible mechanisms underlying the hypertrophic response. Cardiomyocytes isolated from 1-day-old Sprague-Dawley rats were treated with recombinant HMGB1, at concentrations ranging from 50 ng/mL to 200 ng/mL. After 24 hours, cardiomyocytes were processed for the evaluation of atrial natriuretic peptide (ANP) and calcineurin A expression. Western blot and real-time RT-PCR was used to detect protein and mRNA expression levels, respectively. The activity of calcineurin was also evaluated using a biochemical enzyme assay. HMGB1 induced cardiomyocyte hypertrophy, characterized by enhanced expression of ANP, and increased protein synthesis. Meanwhile, increased calcineurin activity and calcineurin A protein expression were observed in cardiomyocytes preconditioned with HMGB1. Furthermore, cyclosporin A pretreatment partially inhibited the HMGB1-induced cardiomyocyte hypertrophy. Our findings suggest that HMGB1 leads to cardiac hypertrophy, at least in part through activating calcineurin.
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