Pathological signaling in the lung induced by particulate matter (PM) air pollution partially overlaps with that provoked by COVID-19, the pandemic disease caused by infection with the novel coronavirus SARS-CoV-2. Metformin is capable of suppressing one of the molecular triggers of the proinflammatory and prothrombotic processes of urban PM air pollution, namely the mitochondrial ROS/Ca 2+ release-activated Ca 2+ channels (CRAC)/IL-6 cascade. Given the linkage between mitochondrial functionality, ion channels, and inflamm-aging, the ability of metformin to target mitochondrial electron transport and prevent ROS/CRAC-mediated IL-6 release might illuminate new therapeutic avenues to quell the raging of the cytokine and thrombotic-like storms that are the leading causes of COVID-19 morbidity and mortality in older people. The incorporation of infection rates, severity and lethality of SARS-CoV-2 infections as new outcomes of metformin usage in elderly populations at risk of developing severe COVID-19, together with the assessment of bronchial/serological titers of inflammatory cytokines and D-dimers, could provide a novel mechanistic basis for the consideration of metformin as a therapeutic strategy against the inflammatory and thrombotic states underlying the gerolavic traits of SARS-CoV-2 infection.
【저자키워드】 COVID-19, Inflammation, aging, Particulate matter, Air pollution, 【초록키워드】 severe COVID-19, IL-6, SARS-COV-2 infection, severity, Infection, lung, risk, cytokine, outcome, Population, metformin, proinflammatory, therapeutic, morbidity and mortality, molecular, therapeutic strategy, Inflammatory cytokine, Inflamm-aging, Signaling, Inflammatory, Trigger, mitochondrial, Transport, Older, overlap, infection rates, novel coronavirus SARS-CoV-2, thrombotic, pandemic disease, cascade, Prevent, prothrombotic, pathological, caused, cause, 【제목키워드】 metformin,