Is the mechanism of COVID-19 coagulopathy still a rabbit's hole?

Ashna Rajan; Ganesh Keshav Thirunavukkarasu; Richard F Lockey; Narasaiah Kolliputi

doi:10.1007/s12079-021-00613-7

Is the mechanism of COVID-19 coagulopathy still a rabbit's hole?

J Cell Commun Signal. 2022 Mar;16(1):1-3. doi: 10.1007/s12079-021-00613-7. Epub 2021 Jun 2.

Authors

Ashna Rajan¹, Ganesh Keshav Thirunavukkarasu², Richard F Lockey³, Narasaiah Kolliputi⁴

Affiliations

¹ Division of Geriatrics Medicine, Brown University Alpert School of Medicine, Providence, RI, 02903, USA.
² Division of Cardiovascular Medicine, Department of Internal Medicine, State University of New York-Downstate Medical Center, Brooklyn, NY, 11203, USA.
³ Division of Allergy and Immunology, Department of Internal Medicine, Morsani College of Medicine, University of South Florida, 2901 Bruce B. Downs Blvd, Tampa, FL, 33612, USA.
⁴ Division of Allergy and Immunology, Department of Internal Medicine, Morsani College of Medicine, University of South Florida, 2901 Bruce B. Downs Blvd, Tampa, FL, 33612, USA. nkollipu@usf.edu.

Abstract

The pathophysiology of COVID-19 is an enigma with its severity often determined by the extent of coagulopathy. Several regulatory pathways targeted by the SARS-CoV-2 include the renin-angiotensin system, von Willebrand Factor, and most importantly, the complement pathway. This article discusses these pathways to help design potential future therapies.

Keywords: ACE2; COVID-19; Coagulopathy; Complement; SARS-CoV2; Thromboinflammation.