FAU own research funding: EFI / IZKF / EAM ...
Start date : 01.01.2021
End date : 30.06.2023
Fibrotic diseases account for 45% of the deaths in the developed world. We demonstrate that the nuclear receptor TR4 is overexpressed in fibrotic tissues in a TGFbeta-dependent manner. TR4 promotes fibroblast-to-myofibroblast transition and collagen release. Knockout of TR4 prevents fibroblast activation and ameliorates experimental fibrosis. In the proposed project, we aim to characterize the molecular mechanisms of fibroblast activation by TR4 and the antifibrotic effects of TR4 inhibition.