Type:

Other

Description:

Two recent genetic studies have identified a critical role for cyclophilin D, a component of the mitochondrial membrane permeability transition pore, in cell death induced by calcium, reactive oxygen species, and cardiac ischemia-reperfusion injury. Transgenic mice lacking cyclophilin D developed normally but showed reduced infarct size after coronary artery ligation and reperfusion. Cells from the knockout mice were resistant to death imposed by excess calcium and H2O2, but not to death from x-irradiation, staurosporine, tumor necrosis factor–α, or forced expression of proapoptotic proteins. These data raise questions about the relationship between apoptotic and necrotic cell death, and they also highlight cyclophilin D as a potential therapeutic target in myocardial infarction.

Subjects:

    Education Levels:

      Keywords:

      CypD,mitochondria,NSDL,NSDL_SetSpec_BEN,signal transduction,mPT,mitochondrial membrane permeability transition,cardiac ischemia-reperfusion injury,Life Science,oai:nsdl.org:2200/20080618215911255T

      Language:

      English

      Access Privileges:

      Public - Available to anyone

      License Deed:

      Creative Commons Attribution Non-Commercial Share Alike

      Collections:

      None
      This resource has not yet been aligned.
      Curriki Rating
      'NR' - This resource has not been rated
      NR
      'NR' - This resource has not been rated

      This resource has not yet been reviewed.

      Not Rated Yet.

      Non-profit Tax ID # 203478467