It is becoming obvious that in addition to aging and various hearth pathologies, excess of body weight, especially obesity is a major risk factor for severity of COVID-19 infection. Intriguingly the receptor for SARS-CoV-2 is ACE2, a member of the angiotensin receptor family that has a relatively large tissue distribution. This observation likely explains the multitude of symptoms that have been described from human patients. The adipose tissue also expresses ACE2, suggesting that adipocytes are potentially infected by SARS-CoV-2. Here we discuss some of the potential contribution of the adipose tissue to the severity of the infection and propose some aspects of obese patients metabolic phenotyping to help stratification of individuals with high risk of severe disease. Highlights • Adipose tissue may be a reservoir for SARS-CoV-2 production. • Obesity-induced chronic inflammatory status generates inappropriate immune response. • Exaggerated-adipose tissue lipolysis in response to proinflammatory cytokines might exert additional lipotoxic effects. • Potential role of adipose-derived products in aggravating COVID-19 infection. • Adipose tissue contribution to COVID-19 severity through the perturbation of local renin angiotensin system.
【저자키워드】 IL, interleukin, COVID-19, Corona virus disease 2019, MERS, Middle East respiratory syndrome, BMI, Body mass index, nAChRs, nicotinic acetylcholine receptors, SARS-COV-2, severe acute respiratory syndrome coronavirus-2, TMPRSS2, Transmembrane Protease Serine 2, PAI-1, plasminogen activator inhibitor-1, ACE2, angiotensin-converting enzyme II, RAS, Renin angiotensin system, NLRP3, NOD-like receptor family pyrin domain containing 3, LDL, low-density lipoprotein, AGT, angiotensinogen, AT, angiotensin receptors, BAT, brown adipose tissue, PD-1, programmed cell death receptor 1, PUFA, polyunsaturated fatty acids, TNFα, tumor necrosis factor-alpha, WAT, white adipose tissue,