.Progress in the Development of Non-cancer Uses of Histone Deacetylase[J] Chinese Pharmaceutical Journal, 2012,V47(5): 321-324
��
[1]
XU W S�� PARMIGIANI R B�� MARKS P A. Histone deacetylase inhibitors: molecular mechanisms of action [J]. Oncogene�� 2007�� 26(37)��5541-5552.[2] WISPLINGHOFF H�� BISCHOFF T�� TALLENT S M�� et al. Nosocomial bloodstream infections in US hospitals: analysis of 24��179 cases from a prospective nationwide surveillance study [J]. Clin Infect Dis�� 2004�� 39(3) ��309-317.[3] PFALLER M A�� DIEKEMA D J. Epidemiology of invasive candidiasis: a persistent public health problem [J]. Clin Microbiol Rev�� 2007�� 20(1) ��133-163.[4] MAI A�� ROTILI D�� MASSA S�� et al. Discovery of uracil-based histone deacetylase inhibitors able to reduce acquired antifungal resistance and trailing growth in Candida albicans [J]. Bioorg Med Chem Lett�� 2007�� 17(5) ��1221-1225.[5] DEMONTE D�� QUIVY V�� COLETTE Y�� et al. Administration of HDAC inhibitors to reactivate HIV-1 expression in latent cellular reservoirs: implications for the development of therapeutic strategies [J]. Biochem Pharmacol�� 2004�� 68(6) ��1231-1238.[6] LEHRMAN G�� HOGUE I B�� PALMER S�� et al. Depletion of latent HIV-1 infection in vivo: a proof-of-concept study [J]. Lancet�� 2005�� 366(9485) ��549-555.[7] World Malaria Day[EB]. World Health Organization�� http://www.who.int/mediacentre/events/annual/malaria/en/index.html.[8] World Malaria Report 2009[R]. World Health Organization�� http://www.who.int/malaria/publications/atoz/9789241563901/en/index.html.[9] KOZIKOWSKI A P�� CHEN Y�� GAYSIN A�� et al. Functional differences in epigenetic modulators-superiority of mercaptoacetamide-based histone deacetylase inhibitors relative to hydroxamates in cortical neuron neuroprotection studies [J]. J Med Chem�� 2007�� 50(13)��3054-3061.[10] ROTILI D�� SIMONETTI G�� SAVARINO A�� et al. Non-cancer uses of histone deacetylase inhibitors: effects on infectious diseases and beta-hemoglobinopathies [J]. Curr Top Med Chem�� 2009�� 9(3)��272-291.[11] ANDREWS K T�� TRAN T N�� WHEATLEY N C�� et al. Targeting histone deacetylase inhibitors for anti-malarial therapy [J]. Curr Top Med Chem�� 2009�� 9(3) ��292-308.[12] DOW G S�� CHEN Y�� ANDREWS K T�� et al. Antimalarial activity of phenylthiazolyl-bearing hydroxamate-based histone deacetylase inhibitors [J]. Antimicrob Agents Chemother�� 2008�� 52(10)��3467-3477.[13] LEVENSON J M�� SWEATT J D. Epigenetic mechanisms in memory formation [J]. Nat Rev Neurosci�� 2005�� 6(2) ��108-118.[14] STEFFAN J S�� BODAI L�� PALLOS J�� et al. Histone deacetylase inhibitors arrest polyglutamine-dependent neurodegeneration in Drosophila [J]. Nature�� 2001�� 413(6857) ��739-743.[15] GARDIAN G�� BROWNE S E�� CHOI D K�� et al. Neuroprotective effects of phenylbutyrate in the N171-82Q transgenic mouse model of Huntington's disease [J]. J Biol Chem�� 2005�� 280(1)��556-563.[16] HAHNEN E�� HAUKE J�� TRANKLE C�� et al. Histone deacetylase inhibitors: possible implications for neurodegenerative disorders [J]. Expert Opin Investig Drugs�� 2008�� 17(2) ��169-184.[17] PETRI S�� KIAEI M�� KIPIANI K�� et al. Additive neuroprotective effects of a histone deacetylase inhibitor and a catalytic antioxidant in a transgenic mouse model of amyotrophic lateral sclerosis [J]. Neurobiol Dis�� 2006�� 22(1)��40-49.[18] RYU H�� SMITH K�� CAMELO S I�� et al. Sodium phenylbutyrate prolongs survival and regulates expression of anti-apoptotic genes in transgenic amyotrophic lateral sclerosis mice [J]. J Neurochem�� 2005�� 93(5) ��1087-1098.[19] SUGAI F�� YAMAMOTO Y�� MIYAGUCHI K�� et al. Benefit of valproic acid in suppressing disease progression of ALS model mice [J]. Eur J Neurosci�� 2004�� 20(11) ��3179-3183.[20] MINAMIYAMA M�� KATSUNO M�� ADACHI H�� et al. Sodium butyrate ameliorates phenotypic expression in a transgenic mouse model of spinal and bulbar muscular atrophy [J]. Hum Mol Genet�� 2004�� 13(11) ��1183-1192.[21] BRICHTA L�� HOLKER I�� HAUG K�� et al. In vivo activation of SMN in spinal muscular atrophy carriers and patients treated with valproate [J]. Ann Neurol�� 2006�� 59(6) ��970-975.[22] KONTOPOULOS E�� PARVIN J D�� FEANY M B�� Alpha-synuclein acts in the nucleus to inhibit histone acetylation and promote neurotoxicity [J]. Hum Mol Genet�� 2006�� 15(20) ��3012-3023.[23] GARDIAN G�� YANG L�� CLEREN C�� et al. Neuroprotective effects of phenylbutyrate against MPTP neurotoxicity [J]. Neuromolecular Med�� 2004�� 5(3) ��235-241.[24] CAO X�� SUDHOF T C. A transcriptionally [correction of transcriptively] active complex of APP with Fe65 and histone acetyltransferase Tip60 [J]. Science�� 2001�� 293(5527) ��115-120.[25] QING H�� HE G�� LY P T�� et al. Valproic acid inhibits Abeta production�� neuritic plaque formation�� and behavioral deficits in Alzheimer's disease mouse models [J]. J Exp Med�� 2008�� 205(12) ��2781-2789.[26] BELYAEV N D�� NALIVAEVA N N�� MAKOVA N Z�� et al. Neprilysin gene expression requires binding of the amyloid precursor protein intracellular domain to its promoter: implications for Alzheimer disease [J]. EMBO Rep�� 2009�� 10(1) ��94-100.[27] FISCHER A�� SANANBENESI F�� WANG X�� et al. Recovery of learning and memory is associated with chromatin remodelling [J]. Nature�� 2007�� 447(7141) ��178-182.[28] RICOBARAZA A�� CUADRADO-TEJEDOR M�� PEREZ-MEDIAVILLA A�� et al. Phenylbutyrate ameliorates cognitive deficit and reduces tau pathology in an Alzheimer's disease mouse model [J]. Neuropsychopharmacology�� 2009�� 34(7) ��1721-1732.[29] REN M�� LENG Y�� JEONG M�� et al. Valproic acid reduces brain damage induced by transient focal cerebral ischemia in rats: potential roles of histone deacetylase inhibition and heat shock protein induction [J]. J Neurochem�� 2004�� 89(6):1358-1367.[30] FARACO G�� PANCANI T�� FORMENTINI L�� et al. Pharmacological inhibition of histone deacetylases by suberoylanilide hydroxamic acid specifically alters gene expression and reduces ischemic injury in the mouse brain [J]. Mol Pharmacol�� 2006�� 70(6) ��1876-1884.[31] ENDRES M�� MEISEL A�� BINISZKIEWICZ D�� et al. DNA Methyltransferase contributes to delayed ischemic brain injury [J]. J Neurosci�� 2000�� 20(9) ��3175-3181.[32] TSANKOVA N�� RENTHAL W�� KUMAR A�� et al. Epigenetic regulation in psychiatric disorders [J]. Nat Rev Neurosci�� 2007�� 8(5) ��355-367.[33] TSANKOVA N M�� BERTON O�� RENTHAL W�� et al. Sustained hippocampal chromatin regulation in a mouse model of depression and antidepressant action [J]. Nat Neurosci�� 2006�� 9(4) ��519-525.[34] SCHROEDER F A�� LIN C L�� CRUSIO W E�� et al. Antidepressant-like effects of the histone deacetylase inhibitor�� sodium butyrate�� in the mouse [J]. Biol Psychiatry�� 2007�� 62(1) ��55-64.[35] WU X�� CHEN P S�� DALLAS S�� et al. Histone deacetylase inhibitors up-regulate astrocyte GDNF and BDNF gene transcription and protect dopaminergic neurons [J]. Int J Neuropsychopharmacol�� 2008�� 11(8) ��1123-1134.[36] CHOO Q Y�� HO P C�� LIN H S. Histone deacetylase inhibitors: new hope for rheumatoid arthritis? [J]. Curr Pharm Des�� 2008�� 14(8) ��803-820.[37] NAKAMURA T�� KUKITA T�� SHOBUIKE T�� et al. Inhibition of histone deacetylase suppresses osteoclastogenesis and bone destruction by inducing IFN-beta production [J]. J Immunol�� 2005�� 175(9) ��5809-5916.[38] GUSTERSON R J�� JAZRAWI E�� ADCOCK I M�� et al. The transcriptional co-activators CREB-binding protein (CBP) and p300 play a critical role in cardiac hypertrophy that is dependent on their histone acetyltransferase activity [J]. J Biol Chem�� 2003�� 278(9) ��6838-6847.[39] KOOK H�� LEPORE J J�� GITLER A D�� et al. Cardiac hypertrophy and histone deacetylase-dependent transcriptional repression mediated by the atypical homeodomain protein Hop [J]. J Clin Invest�� 2003�� 112(6) ��863-871.[40] KONG Y�� TANNOUS P�� LU G�� et al. Suppression of class I and II histone deacetylases blunts pressure-overload cardiac hypertrophy [J]. Circulation�� 2006�� 113(22) ��2579-2588.[41] CHOI J H�� NAM K H�� KIM J�� et al. Trichostatin A exacerbates atherosclerosis in low density lipoprotein receptor-deficient mice [J]. Arterioscler Thromb Vasc Biol�� 2005�� 25(11) ��2404-2409.[42] NALIVAEVA N N�� BELYAEV N D�� TURNER A J. Sodium valproate: an old drug with new roles [J]. Trends Pharm Sci�� 2009�� 30(10) ��509-514.[43] BUTLER R�� BATES G P. Histone deacetylase inhibitors as therapeutics for polyglutamine disorders [J]. Nat Rev Neurosci�� 2006�� 7(10) ��784-796.[44] SIMONINI M V�� CAMARGO L M�� DONG E�� et al. The benzamide MS-275 is a potent�� long-lasting brain region-selective inhibitor of histone deacetylases [J]. Proc Natl Acad Sci USA�� 2006�� 103(5) ��1587-1592.
2012, Vol. 47 
