CITED2 deficiency drives pulmonary hypoplasia via miR-200b and inflammatory pathways
Our data suggest that CITED2 is crucial for fetal lung development, alveolar structure and balanced inflammatory signaling. Both under- (Cited2<sup>-/-</sup>) and overexpression (CDH) of CITED2 result in lung hypoplasia. SoxC family transcription factors were dysregulated in both models of abnormal lung development, which may be related to downstream changes in inflammatory cytokine expression. Evidence supports miR-200b as an upstream regulator of CITED2, which can be targeted in future studies of abnormal lung development and CDH.
Authors
- Marietta Jank (ORCID: https://orcid.org/0000-0002-7064-9687)
- Jai Sareen
- Muntahi Mourin
- Marija Kuna (ORCID: https://orcid.org/0000-0002-5367-731X)
- Yuichiro Miyake (ORCID: https://orcid.org/0000-0003-2391-1205)
- Arzu Ozturk Aptekmann
- Daywin Patel
- Jacquelyn Schwartz
- Michael J. Soares
- Michael Boettcher
- Sakika Shimzu
- Rina Tanaka
- Jackie Wang
Institutions
- Heidelberg University (DE)
- University Hospital Heidelberg (DE)
- Children's Hospital Research Institute of Manitoba (CA)
- University of Kansas Medical Center (US)
- University Medical Centre Mannheim (DE)
- University of Manitoba (CA)
Publication Details
- Journal
- Journal of Pediatric Surgery
- Published
- 2026-02-01
- DOI
- https://doi.org/10.1016/j.jpedsurg.2026.163010
- Primary Topic
- Congenital Diaphragmatic Hernia Studies
- Type
- article
- Field-Weighted Citation Impact
- 0.00
Funders
- Deutsche Forschungsgemeinschaft
- Canadian Institutes of Health Research