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10.1016/j.drudis.2021.03.013

http://scihub22266oqcxt.onion/10.1016/j.drudis.2021.03.013
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33775925!7997138!33775925
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suck abstract from ncbi


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pmid33775925      Drug+Discov+Today 2021 ; 26 (8): 2036-2044
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  • Diabetes, inflammation, and the adiponectin paradox: Therapeutic targets in SARS-CoV-2 #MMPMID33775925
  • Ho G; Ali A; Takamatsu Y; Wada R; Masliah E; Hashimoto M
  • Drug Discov Today 2021[Aug]; 26 (8): 2036-2044 PMID33775925show ga
  • Aging and pre-existing conditions in older patients increase severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) severity and its complications, although the causes remain unclear. Apart from acute pulmonary syndrome, Coronavirus 2019 (COVID-19) can increasingly induce chronic conditions. Importantly, SARS-CoV-2 triggers de novo type 2 diabetes mellitus (T2DM) linked to age-associated cardiovascular disease (CVD), cancers, and neurodegeneration. Mechanistically, SARS-CoV-2 induces inflammation, possibly through damage-associated molecular pattern (DAMP) signaling and 'cytokine storm,' causing insulin resistance and the adiponectin (APN) paradox, a phenomenon linking metabolic dysfunction to chronic disease. Accordingly, preventing the APN paradox by suppressing APN-related inflammatory signaling might prove beneficial. A better understanding could uncover novel therapies for SARS-CoV-2 and its chronic disorders.
  • |*COVID-19/immunology/metabolism[MESH]
  • |*SARS-CoV-2/pathogenicity/physiology[MESH]
  • |Adiponectin/*metabolism[MESH]
  • |Aging/*physiology[MESH]
  • |Chronic Disease[MESH]
  • |Diabetes Mellitus, Type 2/*immunology[MESH]
  • |Humans[MESH]
  • |Inflammation/*metabolism[MESH]


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