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Histone deacetylase (HDAC) inhibition improves myocardial function and prevents cardiac remodeling in diabetic mice

Overview of attention for article published in Cardiovascular Diabetology, August 2015
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Title
Histone deacetylase (HDAC) inhibition improves myocardial function and prevents cardiac remodeling in diabetic mice
Published in
Cardiovascular Diabetology, August 2015
DOI 10.1186/s12933-015-0262-8
Pubmed ID
Authors

Youfang Chen, Jianfeng Du, Yu Tina Zhao, Ling Zhang, Guorong Lv, Shougang Zhuang, Gangjian Qin, Ting C Zhao

Abstract

Recent evidence indicates that inhibition of histone deacetylase (HDAC) protects the heart against myocardial injury and stimulates endogenous angiomyogenesis. However, it remains unknown whether HDAC inhibition produces the protective effect in the diabetic heart. We sought to determine whether HDAC inhibition preserves cardiac performance and suppresses cardiac remodeling in diabetic cardiomyopathy. Adult ICR mice received an intraperitoneal injection of either streptozotocin (STZ, 200 mg/kg) to establish the diabetic model or vehicle to serve as control. Once hyperglycemia was confirmed, diabetic mice received sodium butyrate (1%), a specific HDAC inhibitor, in drinking water on a daily basis to inhibit HDAC activity. Mice were randomly divided into following groups, which includes Control, Control + Sodium butyrate (NaBu), STZ and STZ + Sodium butyrate (NaBu), respectively. Myocardial function was serially assessed at 7, 14, 21 weeks following treatments. Echocardiography demonstrated that cardiac function was depressed in diabetic mice, but HDAC inhibition resulted in a significant functional improvement in STZ-injected mice. Likewise, HDAC inhibition attenuates cardiac hypertrophy, as evidenced by a reduced heart/tibia ratio and areas of cardiomyocytes, which is associated with reduced interstitial fibrosis and decreases in active caspase-3 and apoptotic stainings, but also increased angiogenesis in diabetic myocardium. Notably, glucose transporters (GLUT) 1 and 4 were up-regulated following HDAC inhibition, which was accompanied with increases of GLUT1 acetylation and p38 phosphorylation. Furthermore, myocardial superoxide dismutase, an important antioxidant, was elevated following HDAC inhibition in the diabetic mice. HDAC inhibition plays a critical role in improving cardiac function and suppressing myocardial remodeling in diabetic heart.

Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 88 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 88 100%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 16 18%
Student > Master 13 15%
Student > Doctoral Student 11 13%
Student > Bachelor 8 9%
Researcher 4 5%
Other 8 9%
Unknown 28 32%
Readers by discipline Count As %
Biochemistry, Genetics and Molecular Biology 19 22%
Medicine and Dentistry 16 18%
Pharmacology, Toxicology and Pharmaceutical Science 9 10%
Agricultural and Biological Sciences 5 6%
Psychology 2 2%
Other 5 6%
Unknown 32 36%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 1. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 07 August 2015.
All research outputs
#20,290,425
of 22,826,360 outputs
Outputs from Cardiovascular Diabetology
#1,216
of 1,379 outputs
Outputs of similar age
#220,961
of 264,090 outputs
Outputs of similar age from Cardiovascular Diabetology
#22
of 27 outputs
Altmetric has tracked 22,826,360 research outputs across all sources so far. This one is in the 1st percentile – i.e., 1% of other outputs scored the same or lower than it.
So far Altmetric has tracked 1,379 research outputs from this source. They typically receive more attention than average, with a mean Attention Score of 8.8. This one is in the 1st percentile – i.e., 1% of its peers scored the same or lower than it.
Older research outputs will score higher simply because they've had more time to accumulate mentions. To account for age we can compare this Altmetric Attention Score to the 264,090 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 1st percentile – i.e., 1% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 27 others from the same source and published within six weeks on either side of this one. This one is in the 1st percentile – i.e., 1% of its contemporaries scored the same or lower than it.