Coagulopathy with COVID19 and Tyrosine Kinase Receptor Tie 2: Review Article | ||
| The Egyptian Journal of Hospital Medicine | ||
| Article 169, Volume 91, Issue 1, April 2023, Pages 4847-4842 PDF (584.06 K) | ||
| Document Type: Original Article | ||
| DOI: 10.21608/ejhm.2023.300803 | ||
| Authors | ||
| Esraa Said Fathalla Mohamed* ; Naglaa Ali khalifa; Ayman Fathy Arafa; Weaam Ibrahim Ismail | ||
| Abstract | ||
| Background: The newest coronavirus-caused SARS outbreak was first reported in December 2019 (COVID-19). The Director-General of the World Health Organization declared a global pandemic of COVID-19 three months after the first cases were identified. It is still not apparent how exactly COVID-19 causes coagulopathy, they may be similar to those which cause septic coagulopathy/disseminated intravascular coagulation (DIC) when bacteria are present. Endothelial cells have an abundance of the receptor Tyrosine Kinase Tie2. Additionally, it is expressed by a certain subpopulation of macrophages and has been shown to facilitate angiogenesis. Objective: Review of coagulopathy with COVID19 and Tyrosine Kinase Receptor Tie2. Methods: We scoured scholarly papers and databases including PubMed, Google Scholar, and Science Direct for information on COVID19 and Tyrosine Kinase Receptor. Between March 2016 and February 2023, however, only the latest or most comprehensive study was considered. The authors also assessed the usefulness of references taken from similar books. Documents written in languages other than English have been overlooked because of a lack of funding to translate them. Unpublished articles, oral talks, conference abstracts, and dissertations were all generally agreed upon not to constitute valid scientific investigation. Conclusion: Extreme cases of COVID-19 are characterized by microvascular thrombosis and accompanying endothelial dysfunction. Signaling through the Tie2 receptor helps keep the endothelial surface anticoagulant in a constitutive state. Angiopoietin-2 (Angpt-2) is a prothrombotic phenotypic switch induced by the Tie2 antagonist produced from endothelial cells during inflammation. | ||
| Keywords | ||
| Coagulopathy; COVID-19; Tyrosine kinase receptor | ||
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