{"title":"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","authors":"Ambika Binesh, Kaliyamurthi Venkatachalam","doi":"10.2174/011871529X371965250618060805","DOIUrl":null,"url":null,"abstract":"<p><p>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.</p>","PeriodicalId":93925,"journal":{"name":"Cardiovascular & hematological disorders drug targets","volume":" ","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2025-06-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"IL 6 Cascade in Post COVID Cardiovascular Complications: A Review of Endothelial Injury and Clotting Pathways.\",\"authors\":\"Ambika Binesh, Kaliyamurthi Venkatachalam\",\"doi\":\"10.2174/011871529X371965250618060805\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>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.</p>\",\"PeriodicalId\":93925,\"journal\":{\"name\":\"Cardiovascular & hematological disorders drug targets\",\"volume\":\" \",\"pages\":\"\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2025-06-27\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Cardiovascular & hematological disorders drug targets\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.2174/011871529X371965250618060805\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Cardiovascular & hematological disorders drug targets","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.2174/011871529X371965250618060805","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
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.