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探索 SARS-CoV-2 感染新途径:TRIM25 和 TRIM56 均与 COVID-19 患者的 VEGF、GAS6 和 sAXL 呈正相关。

New Avenues to Explore in SARS-CoV-2 Infection: Both TRIM25 and TRIM56 Positively Correlate with VEGF, GAS6, and sAXL in COVID-19 Patients.

机构信息

Department of Medical Biochemistry, Faculty of Medicine, Erciyes University, Kayseri, Turkey.

Department of Anesthesiology and Reanimation, Faculty of Medicine, Erciyes University, Kayseri, Turkey.

出版信息

Viral Immunol. 2022 Dec;35(10):690-699. doi: 10.1089/vim.2022.0112. Epub 2022 Nov 24.

DOI:10.1089/vim.2022.0112
PMID:36450108
Abstract

The ongoing COVID-19 pandemic poses a significant threat to human health. Many hypotheses regarding pathogenesis have been proposed and are being tried to be clarified by experimental and clinical studies. This study aimed to reveal the roles of the innate immune system modulator GAS6/sAXL pathway, endothelial dysfunction markers vascular endothelial growth factor (VEGF) and hypoxia-inducible factor (HIF)-1, and antiviral effective TRIM25 and TRIM56 proteins in pathogenesis of COVID-19. The study included 55 patients with COVID-19 and 25 healthy individuals. The serum levels of GAS6, sAXL, VEGF, HIF-1, TRIM25, and TRIM56 were measured using commercial ELISA kits and differences between COVID-19 patients and healthy controls, and the relationship to severity and prognosis were evaluated. GAS6, sAXL, TRIM56, and VEGF were found to be higher, while TRIM25 was lower in patients. There were strong positive correlations between GAS6, sAXL, TRIM25, TRIM56, and VEGF. None of the research parameters other than HIF-1 was associated with severity or prognosis. However, HIF-1 was positively correlated with APACHE II. We speculate that the antiviral effective TRIM25 and TRIM56 proteins, as well as the GAS6/sAXL pathway, act together as a defense mechanism in COVID-19. We hope that our study will contribute to further studies to elucidate the molecular mechanism associated with TRIM56, TRIM25, GAS6, sAXL, and VEGF in COVID-19 patients.

摘要

持续的 COVID-19 大流行对人类健康构成重大威胁。许多关于发病机制的假说已经提出,并正在通过实验和临床研究来澄清。本研究旨在揭示先天免疫系统调节剂 GAS6/sAXL 途径、内皮功能障碍标志物血管内皮生长因子 (VEGF) 和缺氧诱导因子 (HIF)-1 以及抗病毒有效蛋白 TRIM25 和 TRIM56 在 COVID-19 发病机制中的作用。该研究纳入了 55 例 COVID-19 患者和 25 名健康个体。使用商业 ELISA 试剂盒测量了血清中的 GAS6、sAXL、VEGF、HIF-1、TRIM25 和 TRIM56 水平,并评估了它们在 COVID-19 患者和健康对照组之间的差异,以及与严重程度和预后的关系。结果发现,COVID-19 患者的 GAS6、sAXL、TRIM56 和 VEGF 水平较高,而 TRIM25 水平较低。GAS6、sAXL、TRIM25、TRIM56 和 VEGF 之间存在强烈的正相关关系。除了 HIF-1 之外,没有其他研究参数与严重程度或预后相关。然而,HIF-1 与 APACHE II 呈正相关。我们推测,抗病毒有效蛋白 TRIM25 和 TRIM56 以及 GAS6/sAXL 途径在 COVID-19 中作为一种防御机制共同发挥作用。我们希望我们的研究将有助于进一步阐明与 COVID-19 患者的 TRIM56、TRIM25、GAS6、sAXL 和 VEGF 相关的分子机制。

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