Human exposure to environmental arsenic induces cardiovascular diseases such as arrhythmias, hypertension, and arteriosclerosis. Here, we review the toxicological and cardiovascular impacts of arsenic in in vitro cardiac and vascular models. The mechanism of arsenic-induced cardiovascular impairments includes oxidative stress, epigenetic modifications, chromatin instability, subcellular damage, and premature aging. The different types of cardiac and vascular cells exhibit distinct responses to arsenic exposure. Arsenic causes arrhythmias, which involve alteration of cardiomyocyte potassium channels and, in turn, repolarization issues. This is mainly due to redox signals that cause epigenetic modifications of potassium channels. On the other hand, vascular lesions, such as damage to blood vessels, occur mainly due to an imbalance in redox levels. This imbalance leads to premature senescence of cells and stop the cell cycle. Furthermore, intracellular accumulation of calcium and ferrous ions plays a major role in arsenic-induced vascular cell apoptosis and cardiomyocyte ferroptosis, respectively.

人体接触环境砷会诱发心律失常、高血压、动脉硬化等心血管疾病。在这里，我们回顾了砷在体外心脏和血管模型中的毒理学和心血管影响。砷引起的心血管损伤的机制包括氧化应激、表观遗传修饰、染色质不稳定、亚细胞损伤和过早衰老。不同类型的心脏和血管细胞对砷暴露表现出不同的反应。砷会导致心律失常，这涉及心肌细胞钾通道的改变，进而导致复极化问题。这主要是由于氧化还原信号引起钾通道的表观遗传修饰。另一方面，血管病变，例如血管损伤，主要是由于氧化还原水平不平衡而发生。这种不平衡导致细胞过早衰老并停止细胞周期。此外，细胞内钙离子和亚铁离子的积累分别在砷诱导的血管细胞凋亡和心肌细胞铁死亡中起主要作用。