Obesity has been recognized as an independent risk factor for critical illness and major severity in subjects with coronavirus disease 2019 (COVID-19). The role of fat distribution, particularly visceral fat (often linked to metabolic abnormalities), is still unclear. The adipose tissue represents a direct source of cytokines responsible for the pathological modifications occurring within adipose tissue in obese subjects. Adipokines are a crucial connection between metabolism and immune system: their dysregulation in obesity contributes to chronic low-grade systemic inflammation and metabolic comorbidities. Therefore the increased amount of visceral fat can lead to a proinflammatory phenotypic shift. This review analyzes the interrelation between obesity and COVID-19 severity, as well as the cellular key players and molecular mechanisms implicated in adipose inflammation, investigating if adipose tissue can constitute a reservoir for viral spread, and contribute to immune activation and cytokines storm. Targeting the underlying molecular mechanisms might have therapeutic potential in the management of obesity-related complications in COVID-19 patients.
【저자키워드】 COVID-19, obesity, Adipose tissue, low-grade inflammation, visceral fat, 【초록키워드】 coronavirus disease, Inflammation, severity, Comorbidities, COVID-19 severity, cytokine, molecular mechanism, viral spread, metabolism, immune, proinflammatory, immune activation, management, Complication, Critical, COVID-19 patients, cellular, Cytokines storm, dysregulation, metabolic abnormalities, connection, tissue, subject, therapeutic potential, obese, independent risk factor, phenotypic, Modification, targeting, adipose, fat, responsible, subjects, contribute, implicated, Adipokine, fat distribution, low-grade systemic inflammation, visceral,