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糖尿病、炎症与脂联素悖论:SARS-CoV-2 的治疗靶点。

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

机构信息

PCND Neuroscience Research Institute, Poway, CA, USA.

Tokyo Metropolitan Institute of Medical Science, 2-1-6 Kamikitazawa, Setagaya-ku, Tokyo, Japan.

出版信息

Drug Discov Today. 2021 Aug;26(8):2036-2044. doi: 10.1016/j.drudis.2021.03.013. Epub 2021 Mar 26.

Abstract

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.

摘要

衰老和老年患者的基础疾病会增加严重急性呼吸综合征冠状病毒 2(SARS-CoV-2)的严重程度及其并发症,尽管其原因仍不清楚。除急性肺综合征外,新型冠状病毒 2019(COVID-19)还会逐渐引起慢性疾病。重要的是,SARS-CoV-2 会引发与年龄相关的心血管疾病(CVD)、癌症和神经退行性变相关的新发 2 型糖尿病(T2DM)。从机制上讲,SARS-CoV-2 会引发炎症,可能通过损伤相关分子模式(DAMP)信号和“细胞因子风暴”来引发胰岛素抵抗和脂联素(APN)悖论,这种现象将代谢功能障碍与慢性疾病联系起来。因此,通过抑制与 APN 相关的炎症信号来预防 APN 悖论可能会有益。更好地理解这一点可能会为 SARS-CoV-2 及其慢性疾病的治疗提供新的途径。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/185e/7997138/749bf61ee4e8/ga1_lrg.jpg

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