COVID-19-driven endothelial damage: complement, HIF-1, and ABL2 are potential pathways of damage and targets for cure.
Monia MarchettiPublished in: Annals of hematology (2020)
COVID-19 pandemia is a major health emergency causing hundreds of deaths worldwide. The high reported morbidity has been related to hypoxia and inflammation leading to endothelial dysfunction and aberrant coagulation in small and large vessels. This review addresses some of the pathways leading to endothelial derangement, such as complement, HIF-1α, and ABL tyrosine kinases. This review also highlights potential targets for prevention and therapy of COVID-19-related organ damage and discusses the role of marketed drugs, such as eculizumab and imatinib, as suitable candidates for clinical trials.
Keyphrases
- coronavirus disease
- sars cov
- endothelial cells
- oxidative stress
- clinical trial
- chronic myeloid leukemia
- public health
- healthcare
- tyrosine kinase
- emergency department
- human health
- respiratory syndrome coronavirus
- randomized controlled trial
- stem cells
- climate change
- health information
- drug induced
- open label
- study protocol