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Published on: February 14, 2017
Dysfunctional Coagulation in COVID-19: From Cell to Bedside
Jie Wang1,2, Ardan M Saguner3, Jiaqi An4,5
1Department of Cardiovascular Medicine, The First Affiliated Hospital of Xi'an Jiaotong University, 277 Yanta West Road, Xi'an, 710061, China.
Abstract:
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes coronavirus disease 2019 (COVID-19), which can induce multisystem disease. Human angiotensin-converting enzyme 2 (ACE2) widely expressing in arterial and venous endothelial cells and arterial smooth muscle cells has been identified as a functional receptor for SARS-CoV-2. Dysfunction of ACE2 leads to abnormal activation of the renin-angiotensin system and a systemic endotheliitis that may relate to abnormal coagulation and sepsis. Meanwhile, innate immune response and inflammation activation participate in dysfunctional coagulation. Previous research indicated that dysfunctional coagulation was one of the important risk factors accountable for a high risk of severe disease and death in patients with COVID-19. Understanding the possible mechanisms of dysfunctional coagulation and appropriate anticoagulation therapeutic strategies are important to prevent disease deterioration and reduce fatality rates during the ongoing COVID-19 pandemic.
Insights
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes COVID-19, leading to multisystem disease and dysfunctional coagulation. Understanding these mechanisms is crucial for developing effective anticoagulation therapies to reduce COVID-19 mortality.
Area of Science:
- Cardiovascular Medicine
- Infectious Diseases
- Hematology
Background:
- Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, causing COVID-19, can result in multisystem disease.
- Human angiotensin-converting enzyme 2 (ACE2) is a key receptor for SARS-CoV-2, and its dysfunction is implicated in COVID-19 pathogenesis.
- Dysfunctional coagulation is a significant risk factor for severe COVID-19 and mortality.
Purpose of the Study:
- To explore the mechanisms linking ACE2 dysfunction, endotheliitis, and innate immune responses to coagulation abnormalities in COVID-19.
- To highlight the importance of understanding these mechanisms for developing effective anticoagulation strategies.
Main Methods:
- Review of existing literature on SARS-CoV-2, ACE2 function, renin-angiotensin system, endotheliitis, and coagulation.
- Analysis of the interplay between innate immunity, inflammation, and coagulation in COVID-19 patients.
Main Results:
- ACE2 dysfunction contributes to renin-angiotensin system abnormalities and systemic endotheliitis.
- Innate immune responses and inflammation play a role in the development of COVID-19-associated coagulopathy.
- Dysfunctional coagulation is a critical factor in COVID-19 severity and fatality.
Conclusions:
- Understanding the complex mechanisms of dysfunctional coagulation in COVID-19 is essential.
- Targeting these mechanisms with appropriate anticoagulation therapies may improve patient outcomes and reduce mortality.
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