Extract
The study reported by Birnhuber et al. [1] in this issue of the European Respiratory Journal addresses the difficulty of assessing pathogenic mechanisms in transgenic animal models of lung pathology and their usefulness in evaluating therapeutic strategies. The authors used mice overexpressing the AP-1 transcription factor Fos-related antigen-2 (Fra-2 transgene/TG), first described in 2008 [2]. In this model, ectopic Fra-2 expression results in fibrosis in various organs, predominantly the lungs [3]. The pulmonary phenotype is characterised by vascular remodelling with pulmonary artery occlusion followed by pulmonary fibrosis.
Abstract
Cell senescence may represent a common trigger to the pulmonary hypertensive, fibrotic and inflammatory phenotype induced by AP-1 overexpression. AP-1 may embody a valuable therapeutic target for pulmonary fibrosis and pulmonary hypertension. https://bit.ly/3EdMbZy
Footnotes
Conflict of interest: All authors have nothing to disclose.
- Received June 26, 2022.
- Accepted September 27, 2022.
- Copyright ©The authors 2022. For reproduction rights and permissions contact permissions{at}ersnet.org
LIBRARY USERS
Log in through your institution
Purchase access
