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10.1152/ajpendo.00198.2020

http://scihub22266oqcxt.onion/10.1152/ajpendo.00198.2020
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suck abstract from ncbi


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pmid32459524      Am+J+Physiol+Endocrinol+Metab 2020 ; 319 (1): E105-E109
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  • Obesity and COVID-19: immune and metabolic derangement as a possible link to adverse clinical outcomes #MMPMID32459524
  • Korakas E; Ikonomidis I; Kousathana F; Balampanis K; Kountouri A; Raptis A; Palaiodimou L; Kokkinos A; Lambadiari V
  • Am J Physiol Endocrinol Metab 2020[Jul]; 319 (1): E105-E109 PMID32459524show ga
  • Recent reports have shown a strong association between obesity and the severity of COVID-19 infection, even in the absence of other comorbidities. After infecting the host cells, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) may cause a hyperinflammatory reaction through the excessive release of cytokines, a condition known as "cytokine storm," while inducing lymphopenia and a disrupted immune response. Obesity is associated with chronic low-grade inflammation and immune dysregulation, but the exact mechanisms through which it exacerbates COVID-19 infection are not fully clarified. The production of increased amounts of cytokines such as TNFalpha, IL-1, IL-6, and monocyte chemoattractant protein (MCP-1) lead to oxidative stress and defective function of innate and adaptive immunity, whereas the activation of NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome seems to play a crucial role in the pathogenesis of the infection. Endothelial dysfunction and arterial stiffness could favor the recently discovered infection of the endothelium by SARS-CoV-2, whereas alterations in cardiac structure and function and the prothrombotic microenvironment in obesity could provide a link for the increased cardiovascular events in these patients. The successful use of anti-inflammatory agents such as IL-1 and IL-6 blockers in similar hyperinflammatory settings, like that of rheumatoid arthritis, has triggered the discussion of whether such agents could be administrated in selected patients with COVID-19 disease.
  • |Adaptive Immunity[MESH]
  • |Betacoronavirus[MESH]
  • |COVID-19[MESH]
  • |Coronavirus Infections/immunology/metabolism/*physiopathology[MESH]
  • |Cytokine Release Syndrome/virology[MESH]
  • |Endothelium/physiopathology[MESH]
  • |Heart/physiopathology/virology[MESH]
  • |Humans[MESH]
  • |Immunity, Innate[MESH]
  • |Inflammation[MESH]
  • |NLR Family, Pyrin Domain-Containing 3 Protein/immunology[MESH]
  • |Obesity/*virology[MESH]
  • |Oxidative Stress[MESH]
  • |Pandemics[MESH]
  • |Pneumonia, Viral/immunology/metabolism/*physiopathology[MESH]
  • |Risk Factors[MESH]
  • |SARS-CoV-2[MESH]
  • |Thrombosis/physiopathology[MESH]


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