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. 2024 May 16;20(5):e1012203.
doi: 10.1371/journal.ppat.1012203. eCollection 2024 May.

Protecting the endothelial glycocalyx in COVID-19

Emira Adam Tay  1 , Vimmal Vijayakumar  1 , Raika Francesca Morales  2 , Ee Soo Lee  3   4 , Andrew Teo  2   3   5
Affiliations

Protecting the endothelial glycocalyx in COVID-19

Emira Adam Tay et al. PLoS Pathog. .
No abstract available

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Conflict of interest statement

The authors have declared that no competing interests exist.

Figures

Fig 1
Fig 1. Diagram depicting the lower respiratory tract, uninfected alveolus (left panel) and infected alveolus (right panel).
Uninfected condition (left panel), in an uninfected condition, the EG regulates the mechanotransduction of flow-induced shear stress in the vascular lumen, promoting a homeostatic environment. SARS-CoV-2 infection (right panel), SARS-CoV-2 infection activates the immune defence to eliminate the pathogen. In the alveolus, activated alveolar macrophages release inflammatory cytokines, driving a local inflammatory response. If unresolved, this inflammation may damage the alveolus. Damaged to the (EG) lining promotes neutrophil migration to the site of infection. Activated neutrophils release antimicrobials such as myeloperoxidase (MPO) and neutrophil extracellular traps, which can damage the glycocalyx. Other sheddases including matrix metalloproteinase (MMP), heparanase, and hyaluronidase, are also released and may further disrupt the glycocalyx integrity. These events damage the pulmonary vasculature, which can lead to fluid buildup in the lungs (pulmonary edema) and respiratory failure. Importantly, a damaged EG also affects mechanotransduction in the circulatory system, potentially altering endothelial cell functions in various organs. This may give rise to multiorgan failure, which is fatal in severe COVID-19 cases. Created with Biorender.
See this image and copyright information in PMC

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