IL - 6级联在COVID后心血管并发症中的作用:内皮损伤和凝血途径的综述

Ambika Binesh, Kaliyamurthi Venkatachalam
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引用次数: 0

摘要

COVID-19大流行揭示了与炎症反应增加有关的各种长期心血管并发症,特别是通过白细胞介素-6 (IL-6)活性增加。IL-6是免疫系统中的一种主要细胞因子,它起着双峰作用:它支持急性免疫防御,但当失调时,它会导致慢性炎症和组织损伤。在COVID-19期间和之后,高水平的IL-6与不良结局有关,如急性呼吸窘迫综合征(ARDS)、心肌炎、内皮功能障碍和血栓形成事件。慢性IL-6信号损害血管稳态,导致内皮功能障碍和血栓增加。病毒和细胞因子驱动的炎症导致COVID-19引起的内皮损伤。这些机制包括ACE2的下调、氧化应激和一氧化氮的生物利用度降低。所有这些都会导致动脉硬化、动脉粥样硬化和血栓形成。有可能通过使用靶向治疗来降低患心脏病的风险,例如可以帮助减少炎症的IL-6抑制剂。内皮健康和炎症的生物标志物包括EPCs和CECs。药物策略,如RAS抑制剂和他汀类药物,可能对内皮功能有附加作用,但ACE2上调仍然是一个主要问题。康复和运动为基础的方法进一步支持血管恢复。当IL-6活性在感染后保持高水平时,它会导致血液太容易凝结并引起血栓形成问题。这使得患者更有可能经历缺血性中风或肺栓塞。抗凝剂和IL-6抑制剂如托珠单抗可降低这些风险。IL-6对心脏的长期影响需要进一步研究,生物标志物筛选、生活方式改变和个性化治疗必须用于尽可能多地预防心脏病。综合抗炎和抗凝策略的整体管理方法将显著改善COVID-19幸存者的预后。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
IL 6 Cascade in Post COVID Cardiovascular Complications: A Review of Endothelial Injury and Clotting Pathways.

The COVID-19 pandemic has revealed various long-term cardiovascular complications linked to increased inflammatory responses, particularly through Interleukin-6 (IL-6) activity. IL-6 is a major cytokine in the immune system that plays a bimodal role: it supports acute immune defense but contributes to chronic inflammation and tissue damage when dysregulated. High levels of IL-6 during and after COVID-19 are linked with poor outcomes, such as Acute Respiratory Distress Syndrome (ARDS), myocarditis, endothelial dysfunction, and thrombotic events. Chronic IL-6 signaling impairs vascular homeostasis, leading to endothelial dysfunction and increased thrombosis. Viral and cytokine-driven inflammation leads to endothelial damage caused by COVID-19. These include mechanisms that implicate the downregulation of ACE2, oxidative stress, and reduced bioavailability of nitric oxide. All these contribute to arterial stiffness, atherosclerosis, and thrombosis. It is possible to reduce the risk of heart disease by using targeted therapies, such as IL-6 inhibitors, which can help reduce inflammation. Biomarkers of endothelial health and inflammation include EPCs and CECs. Pharmacological strategies, such as RAS inhibitors and statins, may have additive effects on endothelial function, but ACE2 upregulation remains a major question. Rehabilitation and exercise-based approaches are further supportive of vascular recovery. When IL-6 activity stays high after an infection, it causes blood to clot too easily and cause thrombotic problems. This makes patients more likely to experience an ischemic stroke or pulmonary embolism. Anticoagulants and IL-6 inhibitors like tocilizumab reduce these risks. IL-6's long-term effects on the heart need to be studied more, and biomarker screening, lifestyle changes, and personalized therapies must be used to prevent heart disease as much as possible. A holistic management approach that integrates anti-inflammatory and anticoagulation strategies will significantly improve outcomes in survivors of COVID-19.

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