ArticleJournal of cellular and molecular medicine2016
Extracellular high-mobility group box 1 mediates pressure overload-induced cardiac hypertrophy and heart failure.
Article in Journal of cellular and molecular medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed.
- Elevated Circulating HMGB1 Levels as a Potential Biomarker for the Diagnosis and Therapy of Heart Failure: A Cross-Sectional Study.Reviews in cardiovascular medicine · 2026Article
- Scoping review of preclinical and clinical studies on the role of HMGB1 in heart disease.NPJ cardiovascular health · 2026Article
- SNX3 mediates heart failure by interacting with HMGB1 and subsequently facilitating its nuclear-cytoplasmic translocation.Acta pharmacologica Sinica · 2025Article
- High Mobility Group Box 1 and Cardiovascular Diseases: Study of Act and Connect.Cardiovascular toxicology · 2024Review
- 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
- T-Cell MyD88 Is a Novel Regulator of Cardiac Fibrosis Through Modulation of T-Cell Activation.Circulation research · 2023Article
- Role of High Mobility Group Box 1 in Cardiovascular Diseases.Inflammation · 2022Review
- MALAT1 regulates hypertrophy of cardiomyocytes by modulating the miR-181a/HMGB2 pathway.European journal of histochemistry : EJH · 2022Article
- Paracrine signal emanating from stressed cardiomyocytes aggravates inflammatory microenvironment in diabetic cardiomyopathy.iScience · 2022Article
- 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
- Trauma, a Matter of the Heart-Molecular Mechanism of Post-Traumatic Cardiac Dysfunction.International journal of molecular sciences · 2021Review
- Recombinant High-Mobility Group Box 1 (rHMGB1) Promotes NRF2-Independent Mitochondrial Fusion through CXCR4/PSMB5-Mediated Drp1 Degradation in Endothelial Cells.Oxidative medicine and cellular longevity · 2021Article
- NETosis as a Pathogenic Factor for Heart Failure.Oxidative medicine and cellular longevity · 2021Review
- High-Mobility Group Box-1 Is Associated With Obesity, Inflammation, and Subclinical Cardiovascular Risk Among Young Adults: A Longitudinal Cohort Study.Arteriosclerosis, thrombosis, and vascular biology · 2020Observational
- Tripartite motif 10 regulates cardiac hypertrophy by targeting the PTEN/AKT pathway.Journal of cellular and molecular medicine · 2020Article
- Effects of Circulating HMGB-1 and Histones on Cardiomyocytes-Hemadsorption of These DAMPs as Therapeutic Strategy after Multiple Trauma.Journal of clinical medicine · 2020Article
- Cardiomyocyte-restricted high-mobility group box 1 (HMGB1) deletion leads to small heart and glycolipid metabolic disorder through GR/PGC-1α signalling.Cell death discovery · 2020Article
- Key Player in Cardiac Hypertrophy, Emphasizing the Role of Toll-Like Receptor 4.Frontiers in cardiovascular medicine · 2020Review
- Inhibition of calpain alleviates coxsackievirus B3-induced myocarditis through suppressing the canonical NLRP3 inflammasome/caspase-1-mediated and noncanonical caspase-11-mediated pyroptosis pathways.American journal of translational research · 2020Article
- Cigarette smoke-induced HMGB1 translocation and release contribute to migration and NF-κB activation through inducing autophagy in lung macrophages.Journal of cellular and molecular medicine · 2020Article
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Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inflammation plays a key role in pressure overload-induced cardiac hypertrophy and heart failure, but the mechanisms have not been fully elucidated. High-mobility group box 1 (HMGB1), which is increased in myocardium under pressure overload, may be involved in pressure overload-induced cardiac injury. The objectives of this study are to determine the role of HMGB1 in cardiac hypertrophy and cardiac dysfunction under pressure overload. Pressure overload was imposed on the heart of male wild-type mice by transverse aortic constriction (TAC), while recombinant HMGB1, HMGB1 box A (a competitive antagonist of HMGB1) or PBS was injected into the LV wall. Moreover, cardiac myocytes were cultured and given sustained mechanical stress. Transthoracic echocardiography was performed after the operation and sections for histological analyses were generated from paraffin-embedded hearts. Relevant proteins and genes were detected. Cardiac HMGB1 expression was increased after TAC, which was accompanied by its translocation from nucleus to both cytoplasm and intercellular space. Exogenous HMGB1 aggravated TAC-induced cardiac hypertrophy and cardiac dysfunction, as demonstrated by echocardiographic analyses, histological analyses and foetal cardiac genes detection. Nevertheless, the aforementioned pathological change induced by TAC could partially be reversed by HMGB1 inhibition. Consistent with the in vivo observations, mechanical stress evoked the release and synthesis of HMGB1 in cultured cardiac myocytes. This study indicates that the activated and up-regulated HMGB1 in myocardium, which might partially be derived from cardiac myocytes under pressure overload, may be of crucial importance in pressure overload-induced cardiac hypertrophy and cardiac dysfunction.
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