Diabetes, inflammation, and the adiponectin paradox: Therapeutic targets in SARS-CoV-2

被引：15
作者：
Ho, Gilbert [1 ]
Ali, Alysha [1 ]
Takamatsu, Yoshiki [2 ]
Wada, Ryoko [2 ]
Masliah, Eliezer [3 ]
Hashimoto, Makoto [2 ]
机构：
[1] PCND Neurosci Res Inst, Poway, CA USA
[2] Tokyo Metropolitan Inst Med Sci, Setagaya Ku, 2-1-6 Kamikitazawa, Tokyo, Japan
[3] NIA, Div Neurosci, NIH, Bethesda, MD 20892 USA
来源：
DRUG DISCOVERY TODAY | 2021年 / 26卷 / 08期
关键词：
COVID-19; SARS-CoV-2; Inflammation; Diabetes mellitus; Adiponectin paradox; Antagonistic pleiotropy; NF-KAPPA-B; NEUTROPHIL EXTRACELLULAR TRAPS; ALARMIN HMGB1; NLRP3; INFLAMMASOME; INSULIN-RESISTANCE; RECEPTOR; ACTIVATION; MORTALITY; COVID-19; EXPRESSION;
D O I：
10.1016/j.drudis.2021.03.013
中图分类号：
R9 [药学];
学科分类号：
1007 ;
摘要：
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.
引用
收藏
页码：2036 / 2044
页数：9
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