Division of Obstetrics and Prenatal Medicine, Department of Gynecology and Obstetrics, University Hospital Frankfurt, J.W. Goethe-University, Theodor-Stern-Kai 7, D-60590 Frankfurt, Germany.
Int J Mol Sci. 2020 Aug 12;21(16):5793. doi: 10.3390/ijms21165793.
The coronavirus disease 2019 COVID-19 pandemic is rapidly spreading worldwide and is becoming a major public health crisis. Increasing evidence demonstrates a strong correlation between obesity and the COVID-19 disease. We have summarized recent studies and addressed the impact of obesity on COVID-19 in terms of hospitalization, severity, mortality, and patient outcome. We discuss the potential molecular mechanisms whereby obesity contributes to the pathogenesis of COVID-19. In addition to obesity-related deregulated immune response, chronic inflammation, endothelium imbalance, metabolic dysfunction, and its associated comorbidities, dysfunctional mesenchymal stem cells/adipose-derived mesenchymal stem cells may also play crucial roles in fueling systemic inflammation contributing to the cytokine storm and promoting pulmonary fibrosis causing lung functional failure, characteristic of severe COVID-19. Moreover, obesity may also compromise motile cilia on airway epithelial cells and impair functioning of the mucociliary escalators, reducing the clearance of severe acute respiratory syndrome coronavirus (SARS-CoV-2). Obese diseased adipose tissues overexpress the receptors and proteases for the SARS-CoV-2 entry, implicating its possible roles as virus reservoir and accelerator reinforcing violent systemic inflammation and immune response. Finally, anti-inflammatory cytokines like anti-interleukin 6 and administration of mesenchymal stromal/stem cells may serve as potential immune modulatory therapies for supportively combating COVID-19. Obesity is conversely related to the development of COVID-19 through numerous molecular mechanisms and individuals with obesity belong to the COVID-19-susceptible population requiring more protective measures.
新型冠状病毒肺炎（COVID-19）疫情在全球迅速蔓延，正在成为一场主要的公共卫生危机。越来越多的证据表明肥胖与 COVID-19 疾病之间存在很强的相关性。我们总结了最近的研究，并从住院、严重程度、死亡率和患者预后等方面探讨了肥胖对 COVID-19 的影响。我们讨论了肥胖导致 COVID-19 发病机制的潜在分子机制。除了肥胖相关的免疫反应失调、慢性炎症、内皮失衡、代谢功能障碍及其相关的合并症外，功能失调的间充质干细胞/脂肪来源的间充质干细胞也可能在促进全身炎症导致细胞因子风暴和促进肺纤维化导致肺功能衰竭方面发挥关键作用，这是严重 COVID-19 的特征。此外，肥胖还可能损害气道上皮细胞的纤毛运动，并损害黏液纤毛清除器的功能，从而减少严重急性呼吸综合征冠状病毒（SARS-CoV-2）的清除。肥胖疾病脂肪组织过度表达 SARS-CoV-2 进入的受体和蛋白酶，暗示其可能作为病毒储存库和加速剂，增强剧烈的全身炎症和免疫反应。最后，抗炎细胞因子如抗白细胞介素 6 和间充质基质/干细胞的给药可能作为支持性治疗 COVID-19 的潜在免疫调节疗法。肥胖通过多种分子机制与 COVID-19 的发生发展相关，肥胖个体属于 COVID-19 易感人群，需要采取更多的保护措施。
