Extract
我们感谢S.Q.李和他的同事们的兴趣in our work [1] and comments allowing us to extend the knowledge gain from our data. Our experiments in cultured human endothelial cells have shown that intermittent hypoxia (IH) directly lead to increased endothelial VE-cadherin cleavage, increased sVE release and endothelial permeability, without involvement of systemic inflammatory processes. Endothelial permeability is a key event in early vascular alterations leading to remodeling and atherosclerosis and it is of crucial importance to decipher this initial process. Although endothelial adhesion markers were already studied in OSA patients [2, 3], this is the first time to our knowledge that VE-cadherin regulation and its consequences in terms of endothelial permeability was addressed in OSA.
Footnotes
This manuscript has recently been accepted for publication in theEuropean Respiratory Journal. It is published here in its accepted form prior to copyediting and typesetting by our production team. After these production processes are complete and the authors have approved the resulting proofs, the article will move to the latest issue of theERJonline. Please open or download the PDF to view this article.
Conflict of interest: Olfa Harki has nothing to disclose.
Conflict of interest: Gilles Faury has nothing to disclose.
Conflict of interest: Isabelle Vilgrain has nothing to disclose.
Conflict of interest: Jean-Louis Pépin has nothing to disclose.
Conflict of interest: Anne Briançon-Marjollet has nothing to disclose.
- AcceptedOctober 11, 2021.
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