SF1: Role of CD248 in mTORC1-mediated unfolded protein response (UPR) in diabetic kidney disease
Initial hypothesis and aims of the project
Based on previously published data and our preliminary data, we hypothesize that CD248 promotes diabetic kidney disease (DKD) by inhibiting the adaptive UPR response, but also by promoting maladaptive signaling. Specifically, we hypothesize that CD248 enhances ATF4 and ATF6α signaling via the UPR, inducing the maladaptive transcription factor CHOP and inflammation by modulating NF-κB signaling. Based on preliminary data and the function of UPR- and mTORC1-signalling in DKD, we also hypothesize that CD248-mediated mTORC1 pathway regulates UPR signaling, thus contributing to renal inflammation and cell death in DKD.
Aims of the project:
Photos: M. Schubert/University Hospital Magdeburg