Centro Andaluz de Biología del Desarrollo, Universidad Pablo de Olavide-CSIC, CIBERER, Instituto de Salud Carlos III, 41013 Sevilla, Spain.
Centro Andaluz de Biología del Desarrollo, Universidad Pablo de Olavide-CSIC, CIBERER, Instituto de Salud Carlos III, 41013 Sevilla, Spain.
Exp Gerontol. 2020 Dec;142:111147. doi: 10.1016/j.exger.2020.111147. Epub 2020 Nov 7.
SARS-CoV-2 causes a severe pneumonia (COVID-19) that affects essentially elderly people. In COVID-19, macrophage infiltration into the lung causes a rapid and intense cytokine storm leading finally to a multi-organ failure and death. Comorbidities such as metabolic syndrome, obesity, type 2 diabetes, lung and cardiovascular diseases, all of them age-associated diseases, increase the severity and lethality of COVID-19. Mitochondrial dysfunction is one of the hallmarks of aging and COVID-19 risk factors. Dysfunctional mitochondria is associated with defective immunological response to viral infections and chronic inflammation. This review discuss how mitochondrial dysfunction is associated with defective immune response in aging and different age-related diseases, and with many of the comorbidities associated with poor prognosis in the progression of COVID-19. We suggest here that chronic inflammation caused by mitochondrial dysfunction is responsible of the explosive release of inflammatory cytokines causing severe pneumonia, multi-organ failure and finally death in COVID-19 patients. Preventive treatments based on therapies improving mitochondrial turnover, dynamics and activity would be essential to protect against COVID-19 severity.
SARS-CoV-2 导致一种严重的肺炎（COVID-19），主要影响老年人。在 COVID-19 中，巨噬细胞浸润肺部导致快速且强烈的细胞因子风暴，最终导致多器官衰竭和死亡。代谢综合征、肥胖、2 型糖尿病、肺部和心血管疾病等合并症都是与年龄相关的疾病，增加了 COVID-19 的严重程度和致死率。线粒体功能障碍是衰老和 COVID-19 危险因素的特征之一。功能失调的线粒体与病毒感染和慢性炎症的免疫反应缺陷有关。本综述讨论了线粒体功能障碍如何与衰老和不同与年龄相关的疾病中的免疫反应缺陷以及与 COVID-19 进展中预后不良相关的许多合并症有关。我们在这里提出，线粒体功能障碍引起的慢性炎症是导致 COVID-19 患者发生严重肺炎、多器官衰竭和最终死亡的炎症细胞因子爆发的原因。基于改善线粒体周转率、动力学和活性的治疗的预防治疗对于预防 COVID-19 的严重程度至关重要。
