Endothelial to mesenchymal transition (EndMT) and vascular remodeling in pulmonary hypertension and idiopathic pulmonary fibrosis

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

“…In the article, authors provide compelling comprehensions from a study comparing post-mortem lung tissues from patients who died from COVID-19 with acute respiratory distress syndrome due to influenza A (H1N1) infection and those with age-matched, uninfected control lungs [ 1 , 2 ]. A crucial inference was the connections between the significant increase in ACE2 positive endothelial cells and the substantial change in endothelial cell morphology, disruption of intercellular junctions, cell swelling, and the breakdown of the underlying basement membrane, all indicative of vascular structural modification in tune to the process of endothelial to mesenchymal transition (EndMT) [ 3 ]. Considering the implications for post-COVID-19 pulmonary fibrosis and vascular destruction seen in this infectious pathology, we believe that the role of EndMT in disease manifestation could be consequential.…”

“…EndMT occurs when endothelial cells respond to an external insult or an internal pathological condition, transforming themselves into a more aggressive mesenchymal state, causing irreversible vascular damage or fibrosis [ 3 ]. The process of EndMT has been considered as one of the major contributors to several other pathological conditions such as pulmonary arterial hypertension, arterial fibrosis, atherosclerosis, cardiac fibrosis, and malignancy [ 3 , 4 ].…”

“…EndMT occurs when endothelial cells respond to an external insult or an internal pathological condition, transforming themselves into a more aggressive mesenchymal state, causing irreversible vascular damage or fibrosis [ 3 ]. The process of EndMT has been considered as one of the major contributors to several other pathological conditions such as pulmonary arterial hypertension, arterial fibrosis, atherosclerosis, cardiac fibrosis, and malignancy [ 3 , 4 ]. Endothelial cells undergoing EndMT loose endothelial characteristics such as a change in morphology, loss of vascular endothelial cadherins (VE-cadherins), CD31 and Tie1/2 with subsequent increase in mesenchymal proteins such as N-cadherin, fibroblast specific protein-1 or S100A4, fibronectin, vimentin, SM22-α, calponin and alpha-smooth muscle actin [ 3 ].…”

“…The process of EndMT has been considered as one of the major contributors to several other pathological conditions such as pulmonary arterial hypertension, arterial fibrosis, atherosclerosis, cardiac fibrosis, and malignancy [ 3 , 4 ]. Endothelial cells undergoing EndMT loose endothelial characteristics such as a change in morphology, loss of vascular endothelial cadherins (VE-cadherins), CD31 and Tie1/2 with subsequent increase in mesenchymal proteins such as N-cadherin, fibroblast specific protein-1 or S100A4, fibronectin, vimentin, SM22-α, calponin and alpha-smooth muscle actin [ 3 ]. As a part of the process basement membrane underlying endothelial cells gets disrupted, facilitating the migration of cells.…”

“…As a part of the process basement membrane underlying endothelial cells gets disrupted, facilitating the migration of cells. This occurs through active proteolytic degradation of basement membrane collagen by matrix metalloproteinases mediated by the transitioning cells [ 3 , 5 ].…”