Copyright
©The Author(s) 2022.
World J Gastroenterol. Jan 21, 2022; 28(3): 275-289
Published online Jan 21, 2022. doi: 10.3748/wjg.v28.i3.275
Published online Jan 21, 2022. doi: 10.3748/wjg.v28.i3.275
COVID-19 and endothelium/blood vessels |
Endothelium and blood vessels are integral parts of COVID-19-induced tissue injury. Their injury is likely due to either direct viral infection and/or cytokine storm triggered by infection of adjacent epithelial cells and inflammatory response[18]. |
Blood vessels are critical for virus dissemination to distant organs. |
Preexisting-impaired endothelial function, e.g., in aging or diabetes are likely predisposing factors COVID-19. Our studies demonstrated that aging gastric mucosa has increased susceptibility to injury and prominent EC abnormalities (decreased VEGF, NGF and impaired mitochondrial function)[19-21]. |
ECs are critical for vascular regeneration (through angiogenesis and vasculogenesis) during injury/lesions healing and therefore are essential for the delivery of oxygen and nutrients to the healing site[22, 23]. |
Several growth factors e.g., NGF, IGF-1, HGF and BMD-stem cells may facilitate tissue regeneration in the healing phase[20,24,25]. |
Long-term effects of COVID-19, its vaccines and treatment on endothelium and vasculature remain to be determined. |
Recently, new oral drugs inhibiting viral replication–Molnupiravir (Merck) and Paxlovid (Pfizer) showed significant efficacy in controlling severe COVID-19 infection by inhibiting viral replication. The interim analysis of the latter drug showed an 89% reduction in risk of COVID-19-related hospitalization or death from any cause compared to placebo in patients treated within three-five days of symptom onset[26]. |
- Citation: Tarnawski AS, Ahluwalia A. Endothelial cells and blood vessels are major targets for COVID-19-induced tissue injury and spreading to various organs. World J Gastroenterol 2022; 28(3): 275-289
- URL: https://www.wjgnet.com/1007-9327/full/v28/i3/275.htm
- DOI: https://dx.doi.org/10.3748/wjg.v28.i3.275