Journal
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY
Volume 130, Issue -, Pages 151-159Publisher
ELSEVIER SCI LTD
DOI: 10.1016/j.yjmcc.2019.04.003
Keywords
Histone deacetylase; HDAC inhibitors; Cardiac hypertrophy; Fibrosis; Metabolism; Heart failure; Diabetic cardiomyopathy
Categories
Funding
- Canadian Institutes of Health Research [FRN-216927]
- The Shine On Foundation
- Baker Heart and Diabetes Institute
Ask authors/readers for more resources
Histone deacetylases (HDACs) regulate gene transcription by catalyzing the removal of acetyl groups from key lysine residues in nucleosomal histones and via the recruitment of other epigenetic regulators to DNA promoter/enhancer regions. Over the past two decades, HDACs have been implicated in multiple processes pertinent to cardiovascular and metabolic diseases, including cardiac hypertrophy and remodeling, fibrosis, calcium handling, inflammation and energy metabolism. The development of small molecule HDAC inhibitors and genetically modified loss- and gain-of-function mouse models has allowed interrogation of the roles of specific HDAC isoforms in these processes. Isoform-selective HDAC inhibitors may prove to be powerful therapeutic agents for the treatment of cardiovascular diseases, obesity and diabetes.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available