ArticleAmerican journal of physiology. Heart and circulatory physiology2008
Negative inotropic effects of high-mobility group box 1 protein in isolated contracting cardiac myocytes.
Article in American journal of physiology. Heart and circulatory physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 64 citations in OpenAlex.
- Conducting polymer-stabilized nanozymes alleviate sepsis-induced myocardial injury by inhibiting iron accumulation and lipid peroxidation.Nature communications · 2026Article
- Plasma-Derived Extracellular Vesicles Inhibit Lipopolysaccharide-Induced Apoptosis and Oxidative Stress in Human AC16 Cardiomyocytes.Current issues in molecular biology · 2026Article
- A Retrospective Observational Study of the Association Between Plasma Levels of Interleukin 8 in 42 Patients with Sepsis-Induced Myocardial Dysfunction at a Single Center Between 2017 and 2020.Medical science monitor : international medical journal of experimental and clinical research · 2021Observational
- Exercise Training: The Holistic Approach in Cardiovascular Prevention.High blood pressure & cardiovascular prevention : the official journal of the Italian Society of Hypertension · 2021Review
- Can the calcium-regulating hormones counteract the detrimental impact of pro-inflammatory damage-associated molecular patterns in the development of heart failure?Journal of investigative medicine : the official publication of the American Federation for Clinical Research · 2021Review
- Comprehensive Mechanism, Novel Markers and Multidisciplinary Treatment of Severe Acute Pancreatitis-Associated Cardiac Injury - A Narrative Review.Journal of inflammation research · 2021Review
- Reappraising the role of inflammation in heart failure.Nature reviews. Cardiology · 2020Review
- HMGB1 enhances mechanical stress-induced cardiomyocyte hypertrophy in vitro via the RAGE/ERK1/2 signaling pathway.International journal of molecular medicine · 2019Article
- 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 mediates hyperglycaemia-induced cardiomyocyte apoptosis via ERK/Ets-1 signalling pathway.Journal of cellular and molecular medicine · 2014Article
- S100A1 is released from ischemic cardiomyocytes and signals myocardial damage via Toll-like receptor 4.EMBO molecular medicine · 2014Article
- Innate immunity and cardiomyocytes in ischemic heart disease.Life sciences · 2014Review
- HMGB1 is an independent predictor of death and heart transplantation in heart failure.Clinical research in cardiology : official journal of the German Cardiac Society · 2012Article
- Heat shock transcription factor 1 inhibits H₂O₂-induced cardiomyocyte death through suppression of high-mobility group box 1.Molecular and cellular biochemistry · 2012Article
- Potentiation of NMDA receptor-dependent cell responses by extracellular high mobility group box 1 protein.PloS one · 2012Article
- High-mobility group box 1 induces calcineurin-mediated cell hypertrophy in neonatal rat ventricular myocytes.Mediators of inflammation · 2012Article
- Chronic kidney disease worsens sepsis and sepsis-induced acute kidney injury by releasing High Mobility Group Box Protein-1.Kidney international · 2011Article
- Innate immune signaling in cardiac ischemia.Nature reviews. Cardiology · 2011Review
- The cardiokine story unfolds: ischemic stress-induced protein secretion in the heart.Trends in molecular medicine · 2011Review
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
Abstract
High-mobility group box 1 (HMGB1) released from necrotic cells or macrophages functions as a late inflammatory mediator and has been shown to induce cardiovascular collapse during sepsis. Thus far, however, the effect(s) of HMGB1 in the heart are not known. We determined the effects of HMGB1 on isolated feline cardiac myocytes by measuring sarcomere shortening in contracting cardiac myocytes, intracellular Ca2+ transients by using fluo-3, and L-type calcium currents by using whole cell perforate configuration of the patch-clamp technique. Treatment of isolated myocytes with HMGB1 (100 ng/ml) resulted in a 70% decrease in sarcomere shortening and a 50% decrease in the height of the peak Ca2+ transient within 5 min (P < 0.01). The immediate negative inotropic effects of HMGB1 on cell contractility and calcium homeostasis were partially reversible upon washout of HMGB1. A significant inhibition of the inward l-type calcium currents was also documented by the patch-clamp technique. HMGB1 induced the PKC-epsilon translocation, and a PKC inhibitor significantly attenuated the negative inotropic effects of HMGB1. These studies show for the first time that HMGB1 impairs sarcomere shortening by decreasing calcium availability in cardiac myocytes through modulating membrane calcium influx and suggest that HMGB1 maybe acts as a novel myocardial depressant factor during cardiac injury.
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