Platelet dysfunction caused by differentially expressed genes as key pathogenic mechanisms in COVID-19.

IF 1.4 4区 医学 Q3 CARDIAC & CARDIOVASCULAR SYSTEMS
Minerva cardiology and angiology Pub Date : 2024-10-01 Epub Date: 2024-05-27 DOI:10.23736/S2724-5683.24.06501-3
Xiaoyong Tan, Xiaojun Gao, Huanhuan Zheng, Hui Yuan, Hong Liu, Qijun Ran, Mao Luo
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Abstract

At the end of 2019, the novel coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) became prevalent worldwide, which brought a heavy medical burden and tremendous economic losses to the world population. In addition to the common clinical respiratory symptoms such as fever, cough and headache, patients with COVID-19 often have hematological diseases, especially platelet dysfunction. Platelet dysfunction usually leads to multiple organ dysfunction, which is closely related to patient severity or mortality. In addition, studies have confirmed significant changes in the gene expression profile of circulating platelets under SARS-CoV-2 infection, which will further lead to changes in platelet function. At the same time, studies have shown that platelets may absorb SARS-COV-2 mRNA independently of ACE2, which further emphasizes the importance of the stability of platelet function in defense against SARS-CoV-2 infection. This study reviewed the relationship between COVID-19 and platelet and SARS-CoV-2 damage to the circulatory system, and further analyzed the significantly differentially expressed mRNA in platelets after infection with SARS-CoV-2 on the basis of previous studies. The top eight hub genes were identified as NLRP3, MT-CO1, CD86, ICAM1, MT-CYB, CASP8, CXCL8 and CXCR4. Subsequently, the effects of SARS-CoV-2 infection on platelet transcript abnormalities and platelet dysfunction were further explored on the basis of 8 hub genes. Finally, the treatment measures of complications caused by platelet dysfunction in patients with COVID-19 were discussed in detail, so as to provide reference for the prevention, diagnosis and treatment of COVID-19.

差异表达基因导致的血小板功能障碍是 COVID-19 的关键致病机制。
2019年底,由严重急性呼吸系统综合征冠状病毒2(SARS-CoV-2)引起的新型冠状病毒病2019(COVID-19)在全球流行,给世界人民带来了沉重的医疗负担和巨大的经济损失。除了发热、咳嗽、头痛等常见的临床呼吸道症状外,COVID-19 患者通常还伴有血液系统疾病,尤其是血小板功能障碍。血小板功能障碍通常会导致多器官功能障碍,这与患者的病情严重程度或死亡率密切相关。此外,研究证实,在感染 SARS-CoV-2 后,循环血小板的基因表达谱发生了显著变化,这将进一步导致血小板功能的改变。同时,研究表明血小板可独立于 ACE2 吸收 SARS-COV-2 mRNA,这进一步强调了血小板功能稳定性在防御 SARS-CoV-2 感染中的重要性。本研究回顾了 COVID-19 与血小板和 SARS-CoV-2 对循环系统损伤的关系,并在以往研究的基础上进一步分析了 SARS-CoV-2 感染后血小板中显著差异表达的 mRNA。结果发现,前八位中枢基因分别为 NLRP3、MT-CO1、CD86、ICAM1、MT-CYB、CASP8、CXCL8 和 CXCR4。随后,在 8 个中心基因的基础上进一步探讨了 SARS-CoV-2 感染对血小板转录本异常和血小板功能障碍的影响。最后,详细探讨了COVID-19患者血小板功能障碍引起并发症的治疗措施,以期为COVID-19的预防、诊断和治疗提供参考。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Minerva cardiology and angiology
Minerva cardiology and angiology CARDIAC & CARDIOVASCULAR SYSTEMS-
CiteScore
2.60
自引率
18.80%
发文量
118
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