Endothelial to mesenchymal transition: a precursor to post-COVID-19 interstitial pulmonary fibrosis and vascular obliteration?

Abstract

Endothelial to mesenchymal transition (EndMT) could lead to post-COVID-19 pulmonary fibrosis and vascular remodelling https://bit.ly/2QqSKxT

FIGURE 1

Histopathological micrographs of pulmonary arteries from idiopathic pulmonary fibrosis (IPF) patients compared to healthy normal controls (original magnification 20×). a, b) Pulmonary arteries after angiotensin-converting enzyme 2 (ACE2) immunostaining, with high expression in intimal, medial and adventitial layers. c, d) Movat pentachrome staining; note the prominent intimal thickening and luminal narrowing. e, f) Pulmonary arteries after immunohistochemistry with S100A4 and g, h) with vimentin antibodies. The artery wall thickening in IPF patients along with increased expression of mesenchymal biomarkers S100A4 and vimentin are suggestive of active endothelial to mesenchymal transition contributing to vascular remodelling. We propose similar pathology could be driven by severe acute respiratory syndrome coronavirus 2 infection (coronavirus disease 2019) through ACE2 expression in the endothelium as shown in panels a and b. IPF tissue was collected under ethics approval from Alfred Health ethics committee (ethics ID: 336-13) and normal control tissues were provided by the James Hogg Lung Registry, the University of British Columbia (ethics ID: H00-50110).