Histone deacetylases inhibitors (HDACis) as novel therapeutic application in various clinical diseases

被引：68

作者：

Qiu, Xiaoyan ^{[1
]}

Xiao, Xiong ^{[1
]}

Li, Nan ^{[1
]}

Li, Yuemin ^{[1
]}

机构：

[1] Southwest Univ, Sch Anim Sci & Technol, 2 Tian Sheng St, Chongqing 400715, Peoples R China

来源：

PROGRESS IN NEURO-PSYCHOPHARMACOLOGY & BIOLOGICAL PSYCHIATRY | 2017年 / 72卷

基金：

中国国家自然科学基金;

关键词：

HDACi; Brain disorders; Cancer; Endometriosis; Cell reprogramming; SUBEROYLANILIDE HYDROXAMIC ACID; SPINAL MUSCULAR-ATROPHY; CELL NUCLEAR TRANSFER; RUBINSTEIN-TAYBI-SYNDROME; IN-VITRO DEVELOPMENT; EXPERIMENTALLY-INDUCED ENDOMETRIOSIS; TRANSGENIC MOUSE MODEL; LONG-TERM-MEMORY; PHASE-II TRIAL; PROTECTS DOPAMINERGIC-NEURONS;

D O I：

10.1016/j.pnpbp.2016.09.002

中图分类号：

R74 [神经病学与精神病学];

学科分类号：

摘要：

Accumulating evidence suggests that histone hypoacetylation which is partly mediated by histone deacetylase (HDAC), plays a causative role in the etiology of various clinical disorders such as cancer and central nervous diseases. HDAC inhibitors (HDACis) are natural or synthetic small molecules that can inhibit the activities of HDACs and restore or increase the level of histone acetylation, thus may represent the potential approach to treating a number of clinical disorders. This manuscript reviewed the progress of the most recent experimental application of HDACis as novel potential drugs or agents in a large number of clinical disorders including various brain disorders including neurodegenerative and neurodevelopmental cognitive disorders and psychiatric diseases like depression, anxiety, fear and schizophrenia, and cancer, endometriosis and cell reprogramming in somatic cell nuclear transfer in human and animal models of disease, and concluded that HDACis as potential novel therapeutic agents could be used alone or in adjunct to other pharmacological agents in various clinical diseases. (C) 2016 Elsevier Inc. All rights reserved.

引用

页码：60 / 72

页数：13

共 283 条

[41] Hippocampal-dependent antidepressant-like activity of histone deacetylase inhibition [J].

Covington, Herbert E., III ;

Vialou, Vincent F. ;

LaPlant, Quincey ;

Ohnishi, Yoshinori N. ;

Nestler, Eric J. .

NEUROSCIENCE LETTERS, 2011, 493 (03) :122-126

[42] Antidepressant Actions of Histone Deacetylase Inhibitors [J].

Covington, Herbert E., III ;

Maze, Ian ;

LaPlant, Quincey C. ;

Vialou, Vincent F. ;

Ohnishi, Yoshinori N. ;

Berton, Olivier ;

Fass, Dan M. ;

Renthal, William ;

Rush, Augustus J., III ;

Wu, Emma Y. ;

Ghose, Subroto ;

Krishnan, Vaishnav ;

Russo, Scott J. ;

Tamminga, Carol ;

Haggarty, Stephen J. ;

Nestler, Eric J. .

JOURNAL OF NEUROSCIENCE, 2009, 29 (37) :11451-11460

[43] Phase II trial of oral vorinostat (suberoylanilide hydroxamic acid) in relapsed diffuse large-B-cell lymphoma [J].

Crump, M. ;

Coiffier, B. ;

Jacobsen, E. D. ;

Sun, L. ;

Ricker, J. L. ;

Xie, H. ;

Frankel, S. R. ;

Randolph, S. S. ;

Cheson, B. D. .

ANNALS OF ONCOLOGY, 2008, 19 (05) :964-969

[44] Phenylbutyrate is a Multifaceted Drug that Exerts Neuroprotective Effects and Reverses the Alzheimer's Disease-like Phenotype of a Commonly Used Mouse Model [J].

Cuadrado-Tejedor, Mar ;

Ricobaraza, Ana L. ;

Torrijo, Rosana ;

Franco, Rafael ;

Garcia-Osta, Ana .

CURRENT PHARMACEUTICAL DESIGN, 2013, 19 (28) :5076-5084

[45] Rare genetic mutations shed light on the pathogenesis of Parkinson disease [J].

Dawson, TM ;

Dawson, VL .

JOURNAL OF CLINICAL INVESTIGATION, 2003, 111 (02) :145-151

[46] Conservation of methylation reprogramming in mammalian development: Aberrant reprogramming in cloned embryos [J].

Dean, W ;

Santos, F ;

Stojkovic, M ;

Zakhartchenko, V ;

Walter, J ;

Wolf, E ;

Reik, W .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2001, 98 (24) :13734-13738

[47] Increased pre-implantation development of cloned bovine embryos treated with 5-aza-2′-deoxycytidine and trichostatin A [J].

Ding, X. ;

Wang, Y. ;

Zhang, D. ;

Wang, Y. ;

Guo, Z. ;

Zhang, Y. .

THERIOGENOLOGY, 2008, 70 (04) :622-630

[48] Histone deacetylase 6 inhibition compensates for the transport deficit in Huntington's disease by increasing tubulin acetylation [J].

Dompierre, Jim P. ;

Godin, Juliette D. ;

Charrin, Benedicte C. ;

Cordelieres, Fabrice P. ;

King, Stephen J. ;

Humbert, Sandrine ;

Saudou, Frederic .

JOURNAL OF NEUROSCIENCE, 2007, 27 (13) :3571-3583

[49] Sodium butyrate enhances the cytotoxic effect of antineoplastic drugs in human lymphoblastic T-cells [J].

dos Santos, M. P. ;

Schwartsmann, G. ;

Roesler, R. ;

Brunetto, A. L. ;

Abujamra, A. L. .

LEUKEMIA RESEARCH, 2009, 33 (02) :218-221

[50]

Duman RS, 1997, ARCH GEN PSYCHIAT, V54, P597

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