病毒感染驱动的Kallikrein-Kinin系统 (KKS) 激活的潜在途径和病理生理影响
Sharton Vinícius Antunes Coelho1, Fabiane Messner Augusto1, Luciana Barros de Arruda1
1Departamento de Virologia, Instituto de Microbiologia Paulo de Góes, Universidade Federal do Rio de Janeiro, Rio de Janeiro 21941-902, Brazil.
Viruses
|February 24, 2024
概括
系统性病毒感染可以破坏微循环和凝血. 通过B2R受体传递信号的kallikrein-kinin系统 (KKS) 和bradykinin (BK) 涉及病毒病原体,表明潜在的治疗点.
科学领域:
- 病毒学 病毒学
- 免疫学 免疫学 免疫学
- 血管生物学 血管生物学
背景情况:
- 系统性病毒感染经常导致微循环和凝血问题.
- 通过B2R受体传递卡利克林-基宁系统 (KKS) 和布拉迪基宁 (BK) 信号在病毒病原发生过程中越来越多地被识别出来.
- 在COVID-19期间发生的血栓事件增加了对KKS激活作为先天免疫反应的兴趣.
研究的目的:
- 审查病毒复制和炎症刺激KKS的机制.
- 探索KKS激活和BK信号对病毒病变的影响.
- 讨论B2R抗剂作为病毒疾病治疗药物的潜力.
主要方法:
- 对KKS,BK,病毒感染和内皮细胞信号传导研究的文献综述.
- 对将病毒复制和炎症与KKS激活联系起来的机制的分析.
- 检查BK受体 (B2R,B1R) 参与病毒病变的证据.
主要成果:
- 病毒感染激活KKS,导致BK水平升高和微血管功能障碍.
- 病毒复制和炎症可以刺激KKS活动和B2R表达.
- 在病毒感染中,BK信号传递有助于血管透性,,血管生成和疼痛.
结论:
- KKS的激活是病毒感染病原发生的一个重要因素.
- 向B2R抗体可能为病毒性出血和呼吸系统疾病提供治疗效益.
- 对KKS调节的进一步研究可能会产生新的抗病毒策略.
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