de Las Heras Natalia, Martín Giménez Virna Margarita, Ferder León, Manucha Walter, Lahera Vicente
Departamento de Fisiología, Facultad de Medicina, Universidad Complutense, 28040 Madrid, Spain.
Instituto de Investigaciones en Ciencias Químicas, Facultad de Ciencias Químicas y Tecnológicas, Universidad Católica de Cuyo, San Juan 5400, Argentina.
Antioxidants (Basel). 2020 Sep 21;9(9):897. doi: 10.3390/antiox9090897.
Due to its high degree of contagiousness and like almost no other virus, SARS-CoV-2 has put the health of the world population on alert. COVID-19 can provoke an acute inflammatory process and uncontrolled oxidative stress, which predisposes one to respiratory syndrome, and in the worst case, death. Recent evidence suggests the mechanistic role of mitochondria and vitamin D in the development of COVID-19. Indeed, mitochondrial dynamics contribute to the maintenance of cellular homeostasis, and its uncoupling involves pathological situations. SARS-CoV-2 infection is associated with altered mitochondrial dynamics with consequent oxidative stress, pro-inflammatory state, cytokine production, and cell death. Furthermore, vitamin D deficiency seems to be associated with increased COVID-19 risk. In contrast, vitamin D can normalize mitochondrial dynamics, which would improve oxidative stress, pro-inflammatory state, and cytokine production. Furthermore, vitamin D reduces renin-angiotensin-aldosterone system activation and, consequently, decreases ROS generation and improves the prognosis of SARS-CoV-2 infection. Thus, the purpose of this review is to deepen the knowledge about the role of mitochondria and vitamin D directly involved in the regulation of oxidative stress and the inflammatory state in SARS-CoV-2 infection. As future prospects, evidence suggests enhancing the vitamin D levels of the world population, especially of those individuals with additional risk factors that predispose to the lethal consequences of SARS-CoV-2 infection.
由于其高度传染性,且几乎与其他病毒不同,严重急性呼吸综合征冠状病毒2(SARS-CoV-2)已使世界人口的健康处于警戒状态。新型冠状病毒肺炎(COVID-19)可引发急性炎症过程和失控的氧化应激,这使人易患呼吸综合征,在最坏的情况下会导致死亡。最近的证据表明线粒体和维生素D在COVID-19发病过程中的作用机制。事实上,线粒体动力学有助于维持细胞稳态,其解偶联涉及病理情况。SARS-CoV-2感染与线粒体动力学改变有关,进而导致氧化应激、促炎状态、细胞因子产生和细胞死亡。此外,维生素D缺乏似乎与COVID-19风险增加有关。相反,维生素D可使线粒体动力学正常化,从而改善氧化应激、促炎状态和细胞因子产生。此外,维生素D可降低肾素-血管紧张素-醛固酮系统的激活,因此减少活性氧生成并改善SARS-CoV-2感染的预后。因此,本综述的目的是加深对线粒体和维生素D在SARS-CoV-2感染中直接参与调节氧化应激和炎症状态作用的认识。作为未来的前景,有证据表明应提高世界人口的维生素D水平,尤其是那些有额外危险因素、易患SARS-CoV-2感染致命后果的个体。