Coronavirus-19, monocyte/macrophage glycolysis and inhibition by melatonin

• Autores: Reiter, R.; Sharma, Ramaswamy; Castillo, Rafael; Marik, Paul E.; Domínguez Rodriguez, Alberto; Cardinali, Daniel Pedro; Tesarik, Jan
• Año de publicación: 2021
• Idioma: inglés
• Tipo de recurso: artículo
• Fuente: Journal of SARS-CoV-2 and Coronavirus Disease. 2021, 2
• Materia: SARS-CoV-2; COVID-19; MELATONINA; FARMACOLOGIA; SISTEMA RESPIRATORIO
• Institución: Pontificia Universidad Católica Argentina

Fil: Reiter, R. Universidad de Texas. Departamento de Sistemas Celulares y Anatomía; Estados Unidos
Fil: Sharma, Ramaswamy. Universidad de Texas. Departamento de Sistemas Celulares y Anatomía; Estados Unidos
Fil: Castillo, Rafael. Academia de líderes de FAME; Filipinas
Fil: Marik, Paul E. Universidad de Virginia. Facultad de Medicina. Departamento de Medicina Interna, Medicina Pulmonar y de Cuidados Intensivos; Estados Unidos
Fil: Domínguez Rodriguez, Alberto. Hospital Universitario de Canarias. Departamento de Cardiología; España
Fil: Cardinali, Daniel Pedro. Pontifica Universidad Católica Argentina. Facultad de Ciencias Médicas; Argentina
Fil: Tesarik, Jan. Clínica MAR&Gen; España
Abstract: Two highly relevant studies related to SARS-CoV-2 and coronavirus disease (COVID-19) and supporting the use of melatonin to prevent and treat this serious infection were published recently. Campos-Codo and colleagues [1] documented experimentally their claim that drugs which specifically target hypoxia inducible factor-1α (HIF-1α) would likely have great therapeutic value in treating COVID-19. The second report is a retrospective analysis based on the clinical experience at the Columbia University Irving Medical Center with the use of drugs to treat respiratory distress in COVID-19-infected patients who required endotracheal intubation [2]. Hyperinflammatory monocytes/macrophages accumulate in abundance in the lower respiratory tract where they play a key role in determining the severity of SARS-CoV-2 infections. Campos-Codo, et al. [1] found that monocytes/macrophages infected with the SARSCoV-2 virus reprogram their metabolism from the conventional mitochondrial oxidative phosphorylation (OXPHOS) to the (usually) pathological cytosolic glycolysis. This so-called Warburg-type metabolism is aided by the inadequately controlled elevated blood glucose levels of diabetic patients, which enhances cellular glycolysis, viral replication and hastens development of a severe respiratory infection resulting from the elevated cytokine release (“cytokine storm”).