Aging mitochondria in the context of SARS-CoV-2: exploring interactions and implications

Abstract

The coronavirus disease 2019 (COVID-19), caused by severe acute respiratorysyndrome coronavirus 2 (SARS-CoV-2), has presented global challenges with adiverse clinical spectrum, including severe respiratory complications andsystemic effects. This review explores the intricate relationship betweenmitochondrial dysfunction, aging, and obesity in COVID-19. Mitochondria arevital for cellular energy provision and resilience against age-relatedmacromolecule damage accumulation. They manage energy allocation incells, activating adaptive responses and stress signals such as redox imbalanceand innate immunity activation. As organisms age, mitochondrial functiondiminishes. Aging and obesity, linked to mitochondrial dysfunction,compromise the antiviral response, affecting the release of interferons, andworsening COVID-19 severity. Furthermore, the development of post-acutesequelae of SARS-CoV-2 infection (PASC), also known as long COVID hasbeen associated with altered energy metabolism, and chronic immunedysregulation derived from mitochondrial dysfunction. Understanding theinterplay between mitochondria, aging, obesity, and viral infections providesinsights into COVID-19 pathogenesis. Targeting mitochondrial health mayoffer potential therapeutic strategies to mitigate severe outcomes and addresslong-term consequences in infected individuals.