High Mobility Group Box 1 and Cardiovascular Diseases: Study of Act and Connect.

IF 3.4 3区 医学 Q2 CARDIAC & CARDIOVASCULAR SYSTEMS Cardiovascular Toxicology Pub Date : 2024-11-01 Epub Date: 2024-09-06 DOI:10.1007/s12012-024-09919-5
Rufaida Wasim, Aditya Singh, Anas Islam, Saad Mohammed, Aamir Anwar, Tarique Mahmood
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Abstract

Cardiovascular disease is the deadly disease that can result in sudden death, and inflammation plays an important role in its onset and progression. High mobility group box 1 (HMGB1) is a nuclear protein that regulates transcription, DNA replication, repair, and nucleosome assembly. HMGB1 is released passively by necrotic tissues and actively secreted by stressed cells. Extracellular HMGB1 functions as a damage associated molecular patterns molecule, producing numerous redox forms that induce a range of cellular responses by binding to distinct receptors and interactors, including tissue inflammation and regeneration. Extracellular HMGB1 inhibition reduces inflammation and is protective in experimental models of myocardial ischemia/reperfusion damage, myocarditis, cardiomyopathies caused by mechanical stress, diabetes, bacterial infection, or chemotherapeutic drugs. HMGB1 administration following a myocardial infarction followed by permanent coronary artery ligation improves cardiac function by stimulating tissue regeneration. HMGB1 inhibits contractility and produces hypertrophy and death in cardiomyocytes, while also stimulating cardiac fibroblast activity and promoting cardiac stem cell proliferation and differentiation. Maintaining normal nuclear HMGB1 levels, interestingly, protects cardiomyocytes from apoptosis by limiting DNA oxidative stress, and mice with HMGB1cardiomyocyte-specific overexpression are partially protected from cardiac injury. Finally, elevated levels of circulating HMGB1 have been linked to human heart disease. As a result, following cardiac damage, HMGB1 elicits both detrimental and helpful responses, which may be due to the formation and stability of the various redox forms, the particular activities of which in this context are mostly unknown. This review covers recent findings in HMGB1 biology and cardiac dysfunction.

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高流动性群体方框 1 与心血管疾病:行动与联系研究。
心血管疾病是可导致猝死的致命疾病,而炎症在其发病和发展过程中扮演着重要角色。高迁移率基团框 1(HMGB1)是一种核蛋白,可调节转录、DNA 复制、修复和核小体组装。HMGB1 由坏死组织被动释放,由受压细胞主动分泌。细胞外 HMGB1 具有损伤相关分子模式分子的功能,可产生多种氧化还原形式,通过与不同的受体和相互作用体结合诱导一系列细胞反应,包括组织炎症和再生。在心肌缺血/再灌注损伤、心肌炎、由机械应力、糖尿病、细菌感染或化疗药物引起的心肌病的实验模型中,细胞外 HMGB1 抑制剂可减少炎症反应并起到保护作用。心肌梗塞后永久性冠状动脉结扎后服用 HMGB1 可刺激组织再生,从而改善心脏功能。HMGB1 可抑制心肌细胞的收缩力并导致其肥大和死亡,同时还可刺激心脏成纤维细胞的活性并促进心脏干细胞的增殖和分化。有趣的是,维持正常的核 HMGB1 水平可通过限制 DNA 氧化应激保护心肌细胞免于凋亡,HMGB1-心肌细胞特异性过表达的小鼠可部分免于心脏损伤。最后,循环中 HMGB1 水平的升高与人类心脏病有关。因此,在心脏损伤后,HMGB1 既能引起有害反应,也能引起有益反应,这可能是由于各种氧化还原形式的形成和稳定性造成的,而在这种情况下,它们的特定活动大多尚不清楚。本综述涵盖了 HMGB1 生物学和心脏功能障碍方面的最新研究成果。
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来源期刊
Cardiovascular Toxicology
Cardiovascular Toxicology 医学-毒理学
CiteScore
6.60
自引率
3.10%
发文量
61
审稿时长
>12 weeks
期刊介绍: Cardiovascular Toxicology is the only journal dedicated to publishing contemporary issues, timely reviews, and experimental and clinical data on toxicological aspects of cardiovascular disease. CT publishes papers that will elucidate the effects, molecular mechanisms, and signaling pathways of environmental toxicants on the cardiovascular system. Also covered are the detrimental effects of new cardiovascular drugs, and cardiovascular effects of non-cardiovascular drugs, anti-cancer chemotherapy, and gene therapy. In addition, Cardiovascular Toxicology reports safety and toxicological data on new cardiovascular and non-cardiovascular drugs.
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