Extract
Atigny et al. raise interesting points in the transcriptomic analysis of CFTR-impaired endothelial cells (ECs) revealing a pro-inflammatory phenotype [1]. Indeed, CFTR impairment in different endothelial models and organisms, and in the absence of concomitant infection, suggests that ECs are an overlooked mediator in the exaggerated pro-inflammatory phenotype observed in cystic fibrosis (CF). Whether endothelial CFTR is involved in other vascular diseases is an intriguing question. Indeed, a recent report indicates a pivotal role of CFTR in pulmonary arterial hypertension (PAH) [2].
Footnotes
This manuscript has recently been accepted for publication in the European 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 the ERJ online. Please open or download the PDF to view this article.
Conflict of interest: Dr. TREPS has nothing to disclose.
Conflict of interest: Siham BOUSFIA has nothing to disclose.
Conflict of interest: Dr. Carmeliet has nothing to disclose.
Conflict of interest: Dr. Witters has nothing to disclose.
- Received June 10, 2021.
- Accepted June 14, 2021.
- Copyright ©The authors 2021. For reproduction rights and permissions contact permissions{at}ersnet.org