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Published on: May 24, 2020
Pathogenic Basis of Thromboinflammation and Endothelial Injury in COVID-19: Current Findings and Therapeutic
Yasutomi Higashikuni1, Wenhao Liu1, Takumi Obana1
1Department of Cardiovascular Medicine, The University of Tokyo, Tokyo 113-8655, Japan.
Insights
Severe COVID-19 involves thromboinflammation and endothelial injury, driven by immune dysregulation and platelet issues. Understanding these mechanisms is key to developing new treatments for severe coronavirus disease 2019 (COVID-19).
Area of Science:
- Immunology
- Pathology
- Virology
Background:
- Coronavirus disease 2019 (COVID-19), caused by SARS-CoV-2, presents mild symptoms in most but severe complications in others.
- Severe cases involve pneumonia, acute respiratory distress syndrome, and thromboembolism, leading to high mortality.
- SARS-CoV-2 employs immune evasion strategies, impacting T and B cell responses.
Purpose of the Study:
- To review the pathogenic basis of thromboinflammation and endothelial injury in COVID-19.
- To highlight the roles of immune responses, platelet activation, and endothelial dysfunction.
- To discuss potential therapeutic targets for COVID-19.
Main Methods:
- Literature review summarizing current knowledge on COVID-19 pathogenesis.
- Analysis of mechanisms including immune dysregulation, platelet hyperactivation, and endothelial dysfunction.
- Exploration of the interplay between these factors and cardiovascular risk.
Main Results:
- SARS-CoV-2 infection triggers dysregulated immune responses, platelet hyperactivation, and endothelial dysfunction.
- These factors interact and are worsened by cardiovascular risk factors.
- These pathological pathways contribute significantly to severe COVID-19 outcomes.
Conclusions:
- Thromboinflammation and endothelial injury are central to severe COVID-19 pathogenesis.
- Targeting immune responses, platelet activation, and endothelial dysfunction offers potential therapeutic avenues.
- Further research into these mechanisms can guide the development of effective COVID-19 treatments.
Abstract:
Coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has become a global pandemic with a great impact on social and economic activities, as well as public health. In most patients, the symptoms of COVID-19 are a high-grade fever and a dry cough, and spontaneously resolve within ten days. However, in severe cases, COVID-19 leads to atypical bilateral interstitial pneumonia, acute respiratory distress syndrome, and systemic thromboembolism, resulting in multiple organ failure with high mortality and morbidity. SARS-CoV-2 has immune evasion mechanisms, including inhibition of interferon signaling and suppression of T cell and B cell responses. SARS-CoV-2 infection directly and indirectly causes dysregulated immune responses, platelet hyperactivation, and endothelial dysfunction, which interact with each other and are exacerbated by cardiovascular risk factors. In this review, we summarize current knowledge on the pathogenic basis of thromboinflammation and endothelial injury in COVID-19. We highlight the distinct contributions of dysregulated immune responses, platelet hyperactivation, and endothelial dysfunction to the pathogenesis of COVID-19. In addition, we discuss potential therapeutic strategies targeting these mechanisms.
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