Obesity and COVID-19: The mTOR pathway as a possible culprit
Obesity and COVID-19: The mTOR pathway as a possible culprit
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DOI：
10.1111/obr.13084
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发表时间：
2020-06-23
期刊：
影响因子：
8.9
通讯作者：
Mojtahedi, Zahra
中科院分区：
文献类型：
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作者：
Bolourian, Alireza;Mojtahedi, Zahra
由单链核糖核酸病毒1引起的冠状病毒病2019年(新冠肺炎)大流行在全球范围内显示出很大的发病率和死亡率差异。2这些差异可以用几个因素来解释，包括年龄、数据准确性和肥胖。2肥胖增加新冠肺炎发病率/死亡率的机制需要全面了解。可能的机制包括相关的共病和通过人类血管紧张素转换酶2(ACE2)增强病毒进入。2 ACE2可能是冠状病毒进入宿主细胞的受体。在脂肪组织中，ACE2的表达水平高于在肺中的表达水平。肥胖个体的脂肪组织体积增加，从而导致更高的血管紧张素转换酶水平，这可能增加他们对新冠肺炎的易感性。研究人员仍在探索其他可能的解释。病毒在很大程度上依赖于宿主细胞的翻译机制，利用受感染细胞的翻译机制来表达病毒蛋白。1某些途径/分子在肥胖宿主中过度激活，并与冠状病毒中的途径/分子共享，可以进一步使肥胖与新冠肺炎的关联合理化。
The coronavirus disease 2019 (COVID-19) pandemic, caused by a single-stranded RNA virus, 1 has demonstrated considerable variations in rate and mortality globally. 2 These variations have been explained by several factors, including age, data accuracy, and obesity. 2 The mechanisms by which obesity increases the rate/mortality of COVID-19 need to be comprehensively understood. Possible mechanisms include associated comorbidities and enhanced virus entry through the human angiotensin-converting enzyme 2 (ACE2). 2 ACE2 is the putative receptor for coronavirus entry into host cells. In adipose tissues, ACE2 expression levels exceed those expressed in the lung. Individuals with obesity present an increased volume of adipose tissues, and consequently higher ACE2 levels, which could increase their susceptibility to COVID-19. 2 Researchers are still exploring other possible explanations. Viruses largely rely on the host cell translation machinery, exploiting the translational apparatus of the infected cell to express viral proteins. 1 Certain pathways/molecules, hyperactivated in obese hosts and shared with those in coronaviruses, could further rationalize the association of obesity with COVID-19.