Extract
F. Antigny and co-workers raise interesting points in their comment on the transcriptomic analysis of cystic fibrosis transmembrane conductance regulator (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].
Abstract
The role of endothelial CFTR dysfunction goes beyond cystic fibrosis by playing a role in pulmonary arterial hypertension https://bit.ly/2UnC7IF
Footnotes
Author contributions: M. Declercq, L. Treps, S. Bousfia, P. Carmeliet and P. Witters wrote the manuscript. L. Treps made the figure. All authors commented on the manuscript.
Conflict of interest: M. Declercq has nothing to disclose.
Conflict of interest: L. Treps has nothing to disclose.
Conflict of interest: S. Bousfia has nothing to disclose.
Conflict of interest: P. Carmeliet has nothing to disclose.
Conflict of interest: P. 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