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Cell-permeable protein therapy for complex I dysfunction |
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| Authors: | Salvatore Pepe Robert M Mentzer Jr Roberta A Gottlieb |
| Institution: | 1. Heart Research, Murdoch Children’s Research Institute, The Royal Children’s Hospital, Melbourne, Australia 2. Department of Paediatrics, University of Melbourne The Royal Children’s Hospital, Melbourne, Australia 3. Department of Surgery, Wayne State University School of Medicine, Detroit, MI, USA 4. Cedars-Sinai Heart Institute and the Barbra Streisand Women’s Heart Center, Cedars-Sinai Medical Center, 8700 Beverly Blvd., Los Angeles, CA, 90048, USA |
| Abstract: | Complex I deficiency is difficult to treat because of the size and complexity of the multi-subunit enzyme complex. Mutations or deletions in the mitochondrial genome are not amenable to gene therapy. However, animal studies have shown that yeast-derived internal NADH quinone oxidoreductase (Ndi1) can be delivered as a cell-permeable recombinant protein (Tat-Ndi1) that can functionally replace complex I damaged by ischemia/reperfusion. Current and future treatment of disorders affecting complex I are discussed, including the use of Tat-Ndi1. |
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