VDAC as a Potential Target in Huntingtons Disease Therapy: The State of the ArtAndonis Karachitos, Daria Grobys and Hanna Kmita*
Laboratory of Bioenergetics, Institute of Molecular Biology and Biotechnology, Adam Mickiewicz University in Poznań, Umultowska 89, 61-614 Poznań, Poland
- *Corresponding Author:
- Hanna Kmita
Laboratory of Bioenergetics, Institute of Molecular Biology and Biotechnology
Faculty of Biology, Adam Mickiewicz University, Umultowska 89
61-614 Poznań, Poland
Tel: +4861 829-5901
E-mail: [email protected]
Received date: November 24, 2015; Accepted date: December 24, 2015; Published date: December 28, 2015
Citation: Karachitos A, Grobys D, Kmita H (2015) VDAC as a Potential Target in Huntingtons Disease Therapy: The State of the Art. Pharmaceut Reg Affairs 4:157. doi: 10.4172/2167-7689.1000157
Copyright: © 2015 Karachitos A, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
It is becoming increasingly evident that mitochondria dysfunction plays an important role in pathogenesis of Huntington’s disease (HD). However, the underlying mechanism is still needs to be explained. The crucial aspect of the explanation is to indicate the upstream events in mitochondria dysfunction that could contribute to HD. In the review we propose the defect of voltage-dependent anion-selective channel (VDAC), as a causative event in HDrelated mitochondria dysfunction. Thus, we propose to consider VDAC as a crucial element in HD etiology and consequently as a reasonable target for therapeutic interventions in HD, based on developing novel therapeutic strategies eliminating mitochondria dysfunction.