Heterozygous <i>Tcf4</i> Deficiency Mitigates Fuchs Endothelial Corneal Dystrophy Progression in a Mouse Model
Heterozygous knockout of Tcf4 significantly suppressed the progression of the FECD phenotype, including guttae formation and endothelial cell loss, in the FECD mouse model. These findings provide in vivo support for TCF4 as a potential therapeutic target for FECD treatment.
Authors
- Naoki Okumura (ORCID: https://orcid.org/0000-0003-2275-5263)
- Ayaka Izumi
- Yuki Oyama (ORCID: https://orcid.org/0000-0003-4579-5487)
- Kaoru Amano (ORCID: https://orcid.org/0000-0002-4346-4791)
- Masahito Ikawa (ORCID: https://orcid.org/0000-0001-9859-6217)
- Satoru Ito (ORCID: https://orcid.org/0000-0001-7885-4653)
- Noriko Koizumi (ORCID: https://orcid.org/0000-0002-6940-1334)
- Taichi Yuasa
- Albert S. Jun (ORCID: https://orcid.org/0000-0001-8650-2279)
- Kotaro Onishi
Institutions
- Doshisha University (JP)
- University of Virginia (US)
- The University of Osaka (JP)
Publication Details
- Journal
- Investigative Ophthalmology & Visual Science
- Published
- 2025-04-08
- DOI
- https://doi.org/10.1167/iovs.66.4.19
- Primary Topic
- Corneal surgery and disorders
- Type
- article
- Field-Weighted Citation Impact
- 0.00