Essential fatty acids and their metabolites in the pathobiology of (coronavirus disease 2019) COVID-19.
Essential fatty acids and their metabolites in the pathobiology of (coronavirus disease 2019) COVID-19.
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必需脂肪酸及其代谢物在COVID-19病理生物学中的作用（2019年冠状病毒病）。
DOI：
10.1016/j.nut.2020.111052
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发表时间：
2021-03
期刊：
影响因子：
--
通讯作者：
Das UN
中科院分区：
文献类型：
--
作者：
Das UN
由SARS-CoV-2(严重急性呼吸综合征冠状病毒2型)引起的新冠肺炎大流行疾病可致命，原因包括肺血管内皮细胞和其他血管的损伤(称为内皮病)、肺泡渗出性炎症和间质炎症、肺泡上皮细胞增殖和透明膜形成，从而导致急性呼吸窘迫综合征导致呼吸衰竭。新冠肺炎与促炎细胞因子白介素6、肿瘤坏死因子-α以及可能的其他细胞因子的过度产生有关。新冠肺炎几乎影响到身体的所有重要器官。SARS-CoV-2病毒通过其刺突蛋白与血管紧张素转换酶2(ACE2)受体结合来攻击鼻腔和支气管上皮细胞和肺细胞。SARS-CoV-2病毒的摄取由宿主细胞的2型跨膜丝氨酸蛋白酶(TMPRSS2)促进，TMPRSS2裂解ACE2并激活刺突蛋白以帮助冠状病毒进入宿主细胞[1]。ACE2和TMPRSS2均由宿主靶细胞表达。SARS-CoV-2感染肺毛细血管内皮细胞，诱导炎症反应(内皮炎)，触发各种血管中的血栓事件。COVID-19诱导T淋巴细胞凋亡，导致严重的淋巴细胞减少，并由于与脾和淋巴结中异常的毛囊外肿瘤坏死因子-a积聚相关的Bcl-6+生发中心B细胞减少而损害淋巴生成[2]。因此，严重新冠肺炎患者体内高水平的肿瘤坏死因子-α不仅会引发“细胞因子风暴”，还会抑制免疫反应[3，4]。在这方面，Torrinhas等人[5]和Sukkar和Bassetti[6]分别提出的建议是相当有趣的，这些建议表明，肠外鱼油的潜在有益作用和在新冠肺炎中诱导酮症。
The pandemic disease of (coronavirus disease 2019) COVID-19 caused by SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2) can be lethal due to damage to the pulmonary vascular endothelial cells and of other vessels (termed endotheliopathy), alveolar exudative inflammation and interstitial inflammation, alveolar epithelium proliferation, and hyaline membrane formation resulting in respiratory failure due to acute respiratory distress syndrome. COVID-19 is associated with excess production of proinflammatory cytokines interleukin-6 (IL-6), tumor necrosis factor-a (TNF-a), and possibly other cytokines. COVID-19 affects almost all vital organs in the body. SARS-CoV-2 virus targets nasal and bronchial epithelial cells and pneumocytes by the binding of its spike protein to the angiotensin-converting enzyme 2 (ACE2) receptor. SARS-CoV-2 virus uptake is promoted by the type 2 transmembrane serine protease (TMPRSS2) of the host cell, which cleaves ACE2 and activates the spike protein to assist the coronavirus’s entry into the host cells [1]. Both ACE2 and TMPRSS2 are expressed by the host target cells. SARS-CoV-2 infects pulmonary capillary endothelial cells, inducing an inflammatory reaction (endotheliitis) that triggers thrombotic events in various blood vessels.COVID-19 induces apoptosis of T lymphocytes to cause severe lymphopenia and impairs lymphopoiesis owing to a reduction in Bcl-6+ germinal center B cells that correlates with aberrant extrafollicular TNF-a accumulation in the spleen and lymph nodes [2]. Thus, high TNF-a levels seen in severe COVID-19 not only cause a “cytokine storm” but also suppresses immune response [3, 4]. In this context, the proposals made by Torrinhas et al [5] and Sukkar and Bassetti [6] suggesting, respectively, the potential beneficial action of parenteral fish oil and induction of ketosis in COVID-19 are rather interesting.
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影响因子：
13.6
作者：
Loynes CA;Lee JA;Robertson AL;Steel MJ;Ellett F;Feng Y;Levy BD;Whyte MKB;Renshaw SA
通讯作者：
Renshaw SA
影响因子：
3.6
作者：
Poloso, Neil J.;Urquhart, Paula;Woodward, David F.
通讯作者：
Woodward, David F.
DOI：
10.1016/j.bbrc.2018.03.096
发表时间：
2018-04-15
影响因子：
3.1
作者：
Park, Hong Jun;Kim, Jiye;Kim, Hyun-Soo
通讯作者：
Kim, Hyun-Soo
影响因子：
6
作者：
Gundala, Naveen K. V.;Naidu, Vegi G. M.;Das, Undurti N.
通讯作者：
Das, Undurti N.
影响因子：
30.5
作者：
Haworth, Oliver;Cernadas, Manuela;Levy, Bruce D.
通讯作者：
Levy, Bruce D.