SIRT2 as a therapeutic target for age-related disorders
- 1 Cell and Molecular Neuroscience Unit, Instituto de Medicina Molecular, Lisboa, Portugal
- 2 Harvard Medical School and MassGeneral Institute for Neurodegenerative Disease, Massachusetts General Hospital, Boston, MA, USA
- 3 Instituto de Fisiologia, Faculdade de Medicina de Lisboa, Lisboa, Portugal
- 4 Department of Neurodegeneration and Restorative Research, Center for Molecular Physiology of the Brain, Universitätsmedizin Göttingen, Göttingen, Germany
Sirtuin proteins are conserved regulators of aging that have recently emerged as important modifiers of several diseases which commonly occur later in life such as cancer, diabetes, cardiovascular, and neurodegenerative diseases. In mammals, there are seven sirtuins (SIRT1-7), which display diversity in subcellular localization and function. SIRT1 has received much of attention due to its possible impact on longevity, while important biological and therapeutic roles of other sirtuins have been underestimated and just recently recognized. Here we focus on SIRT2, a member of the sirtuin family, and discuss its role in cellular and tissue-specific functions. This review summarizes the main scientific advances on SIRT2 protein biology and explores its potential as a therapeutic target for treatment of age-related disorders.
Keywords: SIRT2, aging, metabolic syndrome, cancer, neurodegenerative disorder
Citation: de Oliveira RM, Sarkander J, Kazantsev AG and Outeiro TF (2012) SIRT2 as a therapeutic target for age-related disorders. Front. Pharmacol. 3:82. doi: 10.3389/fphar.2012.00082
Received: 23 December 2011; Paper pending published: 05 March 2012;
Accepted: 14 April 2012; Published online: 03 May 2012.
Edited by:Salvatore Cuzzocrea, University of Messina, Italy
Reviewed by:Won Suk Lee, Pusan National University School of Medicine, South Korea
Armando A. Genazzani, Università del Piemonte Orientale, Italy
Copyright: © 2012 de Oliveira, Sarkander, Kazantsev and Outeiro. This is an open-access article distributed under the terms of the Creative Commons Attribution Non Commercial License, which permits non-commercial use, distribution, and reproduction in other forums, provided the original authors and source are credited.
*Correspondence: Aleksey G. Kazantsev, Harvard Medical School and Mass General Institute for Neurodegenerative Disease, Massachusetts General Hospital, 55 Fruit Street, Boston, MA 02114, USA. e-mail: firstname.lastname@example.org; Tiago Fleming Outeiro, Cell and Molecular Neuroscience Unit, Instituto de Medicina Molecular, 1649-028 Lisboa, Lisboa, Portugal. e-mail: email@example.com