Max Planck Institute for Heart and Lung Research

ALDH2 inhibition reprograms tubular epithelial cell metabolism and promotes renal injury susceptibility

Fatty Acid Oxidation (FAO) dysfunction induces pro-fibrotic transition in tubular epithelial cells (TECs) and contributes to renal fibrosis in chronic kidney disease (CKD); however, the drivers of metabolic reprogramming in TECs remain unclear. We investigate the role of aldehyde...

Small molecule inhibitor of orphan GPCR dimerization improves host defense and blood pressure control in mice

Orphan GPCRs of the GPRC5 family regulate macrophage activity and vascular contractility by dimerizing with other GPCRs, but pharmacological modulation of this process has not been explored. We previously identified the dimerization interface of receptor GPRC5B and show here that...