ArticleJACC. Basic to translational science2019
Cardiac Nuclear High-Mobility Group Box 1 Ameliorates Pathological Cardiac Hypertrophy by Inhibiting DNA Damage Response.
Article in JACC. Basic to translational science, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 35 citations in OpenAlex.
- HMGB1 as a danger signal in vascular remodeling.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2026Review
- E3 Ligases and Deubiquitinases in Controlling High-Mobility Group Box (HMGB) Protein Functions.International journal of molecular sciences · 2026Review
- Scoping review of preclinical and clinical studies on the role of HMGB1 in heart disease.NPJ cardiovascular health · 2026Article
- DNA damage and repair in cardiomyopathy: mechanisms and therapeutic opportunities.American journal of physiology. Heart and circulatory physiology · 2026Review
- 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
- The redox-active defensive Selenoprotein T as a novel stress sensor protein playing a key role in the pathophysiology of heart failure.Journal of translational medicine · 2024Article
- Macrophage-Specific NLRC5 Protects From Cardiac Remodeling Through Interaction With HSPA8.JACC. Basic to translational science · 2023Article
- Effect of hyperhomocysteinemia on a murine model of smoke-induced pulmonary emphysema.Scientific reports · 2022Article
- Resistin deletion protects against heart failure injury by targeting DNA damage response.Cardiovascular research · 2022Article
- The roles of HMGB1-produced DNA gaps in DNA protection and aging biomarker reversal.FASEB bioAdvances · 2022Article
- Autophagic degradation of CCN2 (cellular communication network factor 2) causes cardiotoxicity of sunitinib.Autophagy · 2022Article
- The contribution of the cardiomyocyte to tissue inflammation in cardiomyopathies.Current opinion in physiology · 2021Article
- NETosis as a Pathogenic Factor for Heart Failure.Oxidative medicine and cellular longevity · 2021Review
- GSK3 modulation in acute lung injury, myocarditis and polycystic kidney disease-related aneurysm.Biochimica et biophysica acta. Molecular cell research · 2020Review
- Alpha-lipoic acid protects against pressure overload-induced heart failure via ALDH2-dependent Nrf1-FUNDC1 signaling.Cell death & disease · 2020Article
- Article
- Key Player in Cardiac Hypertrophy, Emphasizing the Role of Toll-Like Receptor 4.Frontiers in cardiovascular medicine · 2020Review
- Nuclear Hmgb1: The Fix for the Failing Heart.JACC. Basic to translational science · 2019Article
Corrections and comments
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Authors and funding
19 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
High-mobility group box 1 (HMGB1) is a deoxyribonucleic acid (DNA)-binding protein associated with DNA repair. Decreased nuclear HMGB1 expression and increased DNA damage response (DDR) were observed in human failing hearts. DNA damage and DDR as well as cardiac remodeling were suppressed in cardiac-specific HMGB1 overexpression transgenic mice after angiotensin II stimulation as compared with wild-type mice. In vitro, inhibition of HMGB1 increased phosphorylation of extracellular signal-related kinase 1/2 and nuclear factor kappa B, which was rescued by DDR inhibitor treatment. DDR inhibitor treatment provided a cardioprotective effect on angiotensin II-induced cardiac remodeling in mice.
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