Literature DB >> 21942627

Therapeutic potential for HDAC inhibitors in the heart.

Timothy A McKinsey1.   

Abstract

Reversible protein acetylation provides a central mechanism for controlling gene expression and cellular signaling events. Two pharmacological inhibitors of protein deacetylation are currently approved for the treatment of human cancer, and numerous follow-on compounds are in clinical development for oncology and non-oncology indications. The inhibitors target members of a family of enzymes known as histone deacetylases (HDACs). Surprisingly, HDAC inhibitors have also been shown to be efficacious in preclinical models of heart failure. This review highlights roles of HDACs in the heart and the therapeutic potential of HDAC inhibitors for the treatment of heart failure.

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Year:  2011        PMID: 21942627     DOI: 10.1146/annurev-pharmtox-010611-134712

Source DB:  PubMed          Journal:  Annu Rev Pharmacol Toxicol        ISSN: 0362-1642            Impact factor:   13.820


  116 in total

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Authors:  Thomas A Wynn; Thirumalai R Ramalingam
Journal:  Nat Med       Date:  2012-07-06       Impact factor: 53.440

2.  HDACs Regulate miR-133a Expression in Pressure Overload-Induced Cardiac Fibrosis.

Authors:  Ludivine Renaud; Lillianne G Harris; Santhosh K Mani; Harinath Kasiganesan; James C Chou; Catalin F Baicu; An Van Laer; Adam W Akerman; Robert E Stroud; Jeffrey A Jones; Michael R Zile; Donald R Menick
Journal:  Circ Heart Fail       Date:  2015-09-14       Impact factor: 8.790

3.  Selective class I histone deacetylase inhibition suppresses hypoxia-induced cardiopulmonary remodeling through an antiproliferative mechanism.

Authors:  Maria A Cavasin; Kim Demos-Davies; Todd R Horn; Lori A Walker; Douglas D Lemon; Nicholas Birdsey; Mary C M Weiser-Evans; Julie Harral; David C Irwin; Adil Anwar; Michael E Yeager; Min Li; Peter A Watson; Raphael A Nemenoff; Peter M Buttrick; Kurt R Stenmark; Timothy A McKinsey
Journal:  Circ Res       Date:  2012-01-26       Impact factor: 17.367

4.  Histone deacetylase inhibition blunts ischemia/reperfusion injury by inducing cardiomyocyte autophagy.

Authors:  Min Xie; Yongli Kong; Wei Tan; Herman May; Pavan K Battiprolu; Zully Pedrozo; Zhao V Wang; Cyndi Morales; Xiang Luo; Geoffrey Cho; Nan Jiang; Michael E Jessen; John J Warner; Sergio Lavandero; Thomas G Gillette; Aslan T Turer; Joseph A Hill
Journal:  Circulation       Date:  2014-01-06       Impact factor: 29.690

5.  Histone deacetylase (HDAC) inhibitor kinetic rate constants correlate with cellular histone acetylation but not transcription and cell viability.

Authors:  Benjamin E L Lauffer; Robert Mintzer; Rina Fong; Susmith Mukund; Christine Tam; Inna Zilberleyb; Birgit Flicke; Allegra Ritscher; Grazyna Fedorowicz; Roxanne Vallero; Daniel F Ortwine; Janet Gunzner; Zora Modrusan; Lars Neumann; Christopher M Koth; Patrick J Lupardus; Joshua S Kaminker; Christopher E Heise; Pascal Steiner
Journal:  J Biol Chem       Date:  2013-07-29       Impact factor: 5.157

Review 6.  Clinical applications of epigenetics in cardiovascular disease: the long road ahead.

Authors:  Stella Aslibekyan; Steven A Claas; Donna K Arnett
Journal:  Transl Res       Date:  2014-04-08       Impact factor: 7.012

Review 7.  Emerging roles for histone deacetylases in pulmonary hypertension and right ventricular remodeling (2013 Grover Conference series).

Authors:  Maria A Cavasin; Kurt R Stenmark; Timothy A McKinsey
Journal:  Pulm Circ       Date:  2015-03       Impact factor: 3.017

Review 8.  HDAC-dependent ventricular remodeling.

Authors:  Min Xie; Joseph A Hill
Journal:  Trends Cardiovasc Med       Date:  2013-03-15       Impact factor: 6.677

Review 9.  Transcriptional pathways and potential therapeutic targets in the regulation of Ncx1 expression in cardiac hypertrophy and failure.

Authors:  Donald R Menick; Mona S Li; Olga Chernysh; Ludivine Renaud; Denise Kimbrough; Harinath Kasiganesan; Santhosh K Mani
Journal:  Adv Exp Med Biol       Date:  2013       Impact factor: 2.622

10.  Transgenic overexpression of active HDAC4 in the heart attenuates cardiac function and exacerbates remodeling in infarcted myocardium.

Authors:  Ling X Zhang; Jianfeng Du; Yu Tina Zhao; Jianguo Wang; Shouyan Zhang; Patrycja M Dubielecka; Lei Wei; Shougang Zhuang; Gangjian Qin; Y Eugene Chin; Ting C Zhao
Journal:  J Appl Physiol (1985)       Date:  2018-10-04
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