Correcting endothelial dysfunction in both human tissue and an elastase-induced murine model of emphysema shows promise in stopping and reversing the course of the disease, according to an international group of researchers.
EC loss and dysfunction were also hallmarks of emphysematous lungs harvested from the elastase-treated mice. The team found that intravenous delivery of healthy lung ECs from genetically identical mice reversed these phenotypes.
“We also found,” continued Dr. Racanelli, “that removing a specific molecule from the cells had a similar result.” In particular the researchers observe that “Leucine-rich a-2-glycoprotein- 1 (LRG1) was a driver of emphysema, and deletion of Lrg1 from endothelial cells rescued vascular rarefaction and alveolar regression.” LRG1 upregulation, they note ,”directly correlated with severity of the COPD phenotype.”
Source: Journal of Experimental Medicine