Epigenetic and Nongenomic Roles for Histone Deacetylases in Heart Failure

  • Weston W. Blakeslee
  • Philip D. Tatman
  • Timothy A. McKinseyEmail author
Part of the Cardiac and Vascular Biology book series (Abbreviated title: Card. vasc. biol.)


Heart failure due to systolic and/or diastolic ventricular dysfunction afflicts millions of people worldwide. Most heart failure drugs target signaling cascades that emanate from the cardiomyocyte cell surface. However, given the ability of numerous receptors to trigger adverse ventricular remodeling, it has been hypothesized that more efficacious therapeutic strategies would be based on inhibition of downstream “nodal” points that integrate upstream signals to convey a common pathway for heart failure pathogenesis. This chapter highlights data suggesting that a family of epigenetic regulatory enzymes, histone deacetylases (HDACs), represent such nodal points. We discuss recent findings that illustrate how HDACs not only control cardiac gene expression via epigenetic regulation, but also serve crucial non-genomic functions in the heart through deacetylation of non-histone proteins.


Cardiac Hypertrophy HDAC Inhibitor Transverse Aortic Constriction Heart Failure Model Cardiac Myofibril 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.



The authors thank Molly K. McKinsey for assistance with graphics. W.W.B. was funded by the University of Colorado Denver Pharmacology Program NIH T32 Training Grant (GM007635), and T.A.M. was supported by grants from the NIH (R01HL116848, R21AG043822, R01HL127240) and American Heart Association (13GRNT14510001).

Conflict of Interest

The authors declare that they have no conflict of interest.


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Copyright information

© Springer International Publishing Switzerland 2016

Authors and Affiliations

  • Weston W. Blakeslee
    • 1
  • Philip D. Tatman
    • 2
    • 3
  • Timothy A. McKinsey
    • 1
    • 2
    • 3
    • 4
    Email author
  1. 1.Department of PharmacologyUniversity of Colorado DenverAuroraUSA
  2. 2.Medical Scientist Training ProgramUniversity of Colorado DenverAuroraUSA
  3. 3.Department of Medicine, Division of CardiologyUniversity of Colorado DenverAuroraUSA
  4. 4.Consortium for Fibrosis Research and TranslationUniversity of Colorado DenverAuroraUSA

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