Evidence is emerging that severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) can infect various organs of the body, including cardiomyocytes and cardiac endothelial cells in the heart. This review focuses on the effects of SARS-CoV-2 in the heart after direct infection that can lead to myocarditis and an outline of potential treatment options. The main points are: (1) Viral entry: SARS-CoV-2 uses specific receptors and proteases for docking and priming in cardiac cells. Thus, different receptors or protease inhibitors might be effective in SARS-CoV-2-infected cardiac cells. (2) Viral replication: SARS-CoV-2 uses RNA-dependent RNA polymerase for replication. Drugs acting against ssRNA(+) viral replication for cardiac cells can be effective. (3) Autophagy and double-membrane vesicles: SARS-CoV-2 manipulates autophagy to inhibit viral clearance and promote SARS-CoV-2 replication by creating double-membrane vesicles as replication sites. (4) Immune response: Host immune response is manipulated to evade host cell attacks against SARS-CoV-2 and increased inflammation by dysregulating immune cells. Efficiency of immunosuppressive therapy must be elucidated. (5) Programmed cell death: SARS-CoV-2 inhibits programmed cell death in early stages and induces apoptosis, necroptosis, and pyroptosis in later stages. (6) Energy metabolism: SARS-CoV-2 infection leads to disturbed energy metabolism that in turn leads to a decrease in ATP production and ROS production. (7) Viroporins: SARS-CoV-2 creates viroporins that lead to an imbalance of ion homeostasis. This causes apoptosis, altered action potential, and arrhythmia.

中文翻译：

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SARS-CoV-2 对心肌的损害：新兴机制和疗法

有证据表明，严重急性呼吸系统综合症冠状病毒 2 (SARS-CoV-2) 可以感染身体的各个器官，包括心脏中的心肌细胞和心脏内皮细胞。本综述重点关注 SARS-CoV-2 在可导致心肌炎的直接感染后对心脏的影响以及潜在治疗方案的概述。主要观点有：（1）病毒进入：SARS-CoV-2利用特异性受体和蛋白酶在心肌细胞中进行对接和启动。因此，不同的受体或蛋白酶抑制剂可能对 SARS-CoV-2 感染的心脏细胞有效。(2)病毒复制：SARS-CoV-2使用依赖于RNA的RNA聚合酶进行复制。作用于心脏细胞的 ssRNA(+) 病毒复制的药物可能是有效的。(3) 自噬和双膜囊泡：SARS-CoV-2 通过创建双膜囊泡作为复制位点来操纵自噬来抑制病毒清除并促进 SARS-CoV-2 复制。(4) 免疫反应：操纵宿主免疫反应来逃避宿主细胞对 SARS-CoV-2 的攻击，并通过调节免疫细胞来增加炎症。必须阐明免疫抑制治疗的效率。(5)程序性细胞死亡：SARS-CoV-2早期抑制程序性细胞死亡，后期诱导细胞凋亡、坏死和细胞焦亡。(6) 能量代谢：SARS-CoV-2 感染导致能量代谢紊乱，进而导致 ATP 产生和 ROS 产生减少。(7) 病毒孔蛋白：SARS-CoV-2 会产生病毒孔蛋白，导致离子稳态失衡。这会导致细胞凋亡、动作电位改变和心律失常。