title: Halting renal fibrosis: an unexpected role for mTORC2 signaling.
abstract: Slowly progressive renal fibrosis is the hallmark of chronic kidney disease, independent of its etiology. Transforming growth factor-β (TGF-β) has been found to be the main profibrotic renal cytokine. Li et al. identify mTORC2 as an important mediator of TGF-β signaling. Being upstream of the previously described profibrotic kinases AKT, SGK1, and PKC-α, mTORC2 represents a potentially interesting drug target. Yet, although the mouse genetic approach yielded convincing results, transition from bench to bedside will remain challenging.
authors: Renal Division, University Medical Center Freiburg, Freiburg, Germany.
authors: Florian
authors: F
authors: Grahammer
mesh_terms: D000818:Animals; D002352:Carrier Proteins / Q000378:metabolism*; D005347:Fibroblasts / Q000187:drug effects*; D007668:Kidney / Q000187:drug effects*; D007674:Kidney Diseases / Q000201:enzymology*; D008297:Male; D046912:Multiprotein Complexes / Q000378:metabolism*; D015398:Signal Transduction / Q000187:drug effects*; D058570:TOR Serine-Threonine Kinases / Q000378:metabolism*; D053773:Transforming Growth Factor beta1 / Q000494:pharmacology*
chemical_list: D002352:Carrier Proteins; D046912:Multiprotein Complexes; D053773:Transforming Growth Factor beta1; D058570:TOR Serine-Threonine Kinases