tetano
Editor, Senior Moderator
Aging (Albany NY)
. 2020 May 27;12.
doi: 10.18632/aging.103347. Online ahead of print.
Metformin and SARS-CoV-2: Mechanistic Lessons on Air Pollution to Weather the Cytokine/Thrombotic Storm in COVID-19
Javier A Menendez[SUP] 1 2 [/SUP]
Affiliations
Abstract
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[SUP]2+[/SUP] release-activated Ca[SUP]2+[/SUP] 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.
Keywords: COVID-19; aging; air pollution; inflammation; particulate matter.
. 2020 May 27;12.
doi: 10.18632/aging.103347. Online ahead of print.
Metformin and SARS-CoV-2: Mechanistic Lessons on Air Pollution to Weather the Cytokine/Thrombotic Storm in COVID-19
Javier A Menendez[SUP] 1 2 [/SUP]
Affiliations
- PMID: 32463794
- DOI: 10.18632/aging.103347
Abstract
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[SUP]2+[/SUP] release-activated Ca[SUP]2+[/SUP] 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.
Keywords: COVID-19; aging; air pollution; inflammation; particulate matter.