Foglio Eleonora, Pellegrini Laura, Germani Antonia, Russo Matteo Antonio, Limana Federica
Department of Experimental Medicine, Sapienza University of Rome, Rome, Italy.
Institute of Oncology Research (IOR), Bellinzona, Switzerland.
Vasc Biol. 2019 Aug 12;1(1):H89-H96. doi: 10.1530/VB-19-0013. eCollection 2019.
Acute myocardial infarction (MI) and its consequences are the most common and lethal heart syndromes worldwide and represent a significant health problem. Following MI, apoptosis has been generally seen as the major contributor of the cardiomyocyte fate and of the resultant myocardial remodeling. However, in recent years, it has been discovered that, following MI, cardiomyocytes could activate autophagy in an attempt to protect themselves against ischemic stress and to preserve cardiac function. Although initially seen as two completely separate responses, recent works have highlighted the intertwined crosstalk between apoptosis and autophagy. Numerous researches have tried to unveil the mechanisms and the molecular players involved in this phenomenon and have identified in high-mobility group box 1 (HMGB1), a highly conserved non-histone nuclear protein with important roles in the heart, one of the major regulator. Thus, the aim of this mini review is to discuss how HMGB1 regulates these two responses in ischemic heart diseases. Indeed, a detailed understanding of the crosstalk between apoptosis and autophagy in these pathologies and how HMGB1 regulates them would be of tremendous help in developing novel therapeutic approaches aimed to promote cardiomyocyte survival and to diminish tissue injury following MI.
急性心肌梗死（MI）及其后果是全球最常见且致命的心脏综合征，是一个重大的健康问题。心肌梗死后，细胞凋亡通常被视为心肌细胞命运及由此导致的心肌重塑的主要促成因素。然而，近年来发现，心肌梗死后，心肌细胞可激活自噬，试图保护自身免受缺血应激并维持心脏功能。尽管最初被视为两种完全独立的反应，但最近的研究突出了细胞凋亡与自噬之间相互交织的串扰。众多研究试图揭示这一现象所涉及的机制和分子参与者，并确定高迁移率族蛋白B1（HMGB1）是主要调节因子之一，HMGB1是一种高度保守的非组蛋白核蛋白，在心脏中具有重要作用。因此，本综述的目的是讨论HMGB1如何在缺血性心脏病中调节这两种反应。事实上，详细了解这些病理状态下细胞凋亡与自噬之间的串扰以及HMGB1如何对其进行调节，将对开发旨在促进心肌细胞存活并减少心肌梗死后组织损伤的新型治疗方法有极大帮助。
