Background

Globally, the current medical emergency for novel coronavirus 2019 (COVID-19) leads to respiratory distress syndrome and death.

Purpose

This review highlighted the effect of COVID-19 on systemic multiple organ failure syndromes. This review is intended to fill a gap in information about human physiological response to COVID-19 infections. This review may shed some light on other potential mechanisms and approaches in COVID -19 infections towards systemic multiorgan failure syndromes.

Finding

SARS-CoV-2 intervened mainly in the lung with progression to pneumonia and acute respiratory distress syndrome (ARDS) via the angiotensin-converting enzyme 2(ACE2) receptor. Depending on the viral load, infection spread through the ACE2 receptor further to various organs such as heart, liver, kidney, brain, endothelium, GIT, immune cell, and RBC (thromboembolism). This may be aggravated by cytokine storm with the extensive release of proinflammatory cytokines from the deregulating immune system.

Conclusion

The widespread and vicious combinations of cytokines with organ crosstalk contribute to systemic hyper inflammation and ultimately lead to multiple organ dysfunction (Fig. 1). This comprehensive study comprises various manifestations of different organs in COVID-19 and may assist the clinicians and scientists pertaining to a broad approach to fight COVID 19.

中文翻译：

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血管紧张素转换酶 2 (ACE2)：COVID 19 导致多器官衰竭综合征的途径。

背景

在全球范围内，当前针对新型冠状病毒 2019 (COVID-19) 的医疗紧急情况导致呼吸窘迫综合征和死亡。

目的

这篇综述强调了 COVID-19 对全身性多器官衰竭综合征的影响。本综述旨在填补有关人类对 COVID-19 感染的生理反应的信息空白。这篇综述可能会阐明 COVID -19 感染导致系统性多器官衰竭综合征的其他潜在机制和方法。

发现

SARS-CoV-2 主要通过血管紧张素转换酶 2 (ACE2) 受体干预肺部并发展为肺炎和急性呼吸窘迫综合征 (ARDS)。根据病毒载量，感染通过 ACE2 受体进一步传播到各种器官，例如心脏、肝脏、肾脏、大脑、内皮细胞、胃肠道、免疫细胞和红细胞（血栓栓塞）。细胞因子风暴可能会加剧这种情况，因为放松管制的免疫系统会大量释放促炎细胞因子。

结论

细胞因子与器官串扰的广泛和恶性组合导致全身性过度炎症，并最终导致多器官功能障碍（图 1）。这项综合研究包括 COVID-19 中不同器官的各种表现，可能有助于临床医生和科学家采用广泛的方法来对抗 COVID-19。