Rapamycin Attenuates Cardiac Fibrosis in Experimental Uremic Cardiomyopathy by Reducing Marinobufagenin Levels and Inhibiting Downstream Pro-Fibrotic Signaling Article (Faculty180)

cited authors

  • Haller, S T; Yan, Yanling; Drummond, Christopher A; Xie, Joe; Tian, Jiang; Kennedy, David J; Shilova, Victoria Y; Xie, Zijian; Liu, Jiang; Cooper, Christopher J; Malhotra, Deepak; Shapiro, Joseph I; Fedorova, Olga V; Bagrov, Alexei Y


  • Experimental uremic cardiomyopathy causes cardiac fibrosis and is causally related to the increased circulating levels of the cardiotonic steroid, marinobufagenin (MBG), which signals through Na/K-ATPase. Rapamycin is an inhibitor of the serine/threonine kinase mammalian target of rapamycin (mTOR) implicated in the progression of many different forms of renal disease. Given that Na/K-ATPase signaling is known to stimulate the mTOR system, we speculated that the ameliorative effects of rapamycin might influence this pathway.

publication date

  • 2016


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