Histone deacetylase activity governs diastolic dysfunction through a nongenomic mechanism-Reference-Cited by-同舟云学术

Histone deacetylase activity governs diastolic dysfunction through a nongenomic mechanism

Published:2018-02-07 Issue:427 Volume:10 Page:
ISSN:1946-6234
Container-title:Science Translational Medicine
language:en
Short-container-title:Sci. Transl. Med.

Author:

Jeong Mark Y.¹²^ORCID,Lin Ying H.¹²^ORCID,Wennersten Sara A.¹²^ORCID,Demos-Davies Kimberly M.¹^ORCID,Cavasin Maria A.¹²,Mahaffey Jennifer H.¹²^ORCID,Monzani Valmen³,Saripalli Chandrasekhar⁴^ORCID,Mascagni Paolo³^ORCID,Reece T. Brett⁵,Ambardekar Amrut V.¹²^ORCID,Granzier Henk L.⁴,Dinarello Charles A.⁶,McKinsey Timothy A.¹²^ORCID

Affiliation:

1. Division of Cardiology, Department of Medicine, University of Colorado Anschutz Medical Campus, Aurora, CO 80045, USA.

2. Consortium for Fibrosis Research & Translation, University of Colorado Anschutz Medical Campus, Aurora, CO 80045, USA.

3. Italfarmaco S.p.A., Cinisello Balsamo, Italy.

4. Department of Cellular and Molecular Medicine and Sarver Molecular Cardiovascular Research Program, University of Arizona, Tucson, AZ 85724, USA.

5. Division of Cardiothoracic Surgery, Department of Surgery, University of Colorado Anschutz Medical Campus, Aurora, CO 80045, USA.

6. Division of Infectious Diseases, Department of Medicine, University of Colorado Anschutz Medical Campus, Aurora, CO 80045, USA.

Abstract

The histone deacetylase inhibitor ITF2357 (givinostat) prevents diastolic dysfunction by enhancing cardiac myofibril relaxation.

Funder

National Institutes of Health

American Heart Association

Publisher

American Association for the Advancement of Science (AAAS)

Subject

General Medicine

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