Related Experiment Video
Updated: Apr 5, 2026
Mouse Electroacupuncture Fixation Device Fabrication for Electroacupuncture Pretreatment in Diabetic Cardiomyopathy Mouse Model
Published on: April 18, 2025
Histone deacetylase (HDAC) inhibition improves myocardial function and prevents cardiac remodeling in diabetic mice
Youfang Chen1, Jianfeng Du2, Yu Tina Zhao3
1Department of Surgery, Boston University Medical School, Roger Williams Medical Center, Boston University, 50 Maude Street, Providence, RI, 02908, USA. cyf988@126.com.
Insights
Histone deacetylase (HDAC) inhibition improves heart function and reduces cardiac remodeling in diabetic cardiomyopathy. This study shows HDAC inhibition offers protection against diabetic heart injury.
Area of Science:
- Cardiovascular Biology
- Molecular Medicine
- Diabetology
Background:
- Histone deacetylase (HDAC) inhibition shows cardioprotective effects and promotes angiogenesis.
- The impact of HDAC inhibition on the diabetic heart remains unclear.
- Diabetic cardiomyopathy is a significant clinical concern.
Purpose of the Study:
- To investigate the efficacy of HDAC inhibition in preserving cardiac function in diabetic cardiomyopathy.
- To determine if HDAC inhibition can suppress cardiac remodeling in a diabetic mouse model.
Main Methods:
- A diabetic mouse model was established using streptozotocin (STZ).
- Diabetic mice were treated with sodium butyrate (NaBu), an HDAC inhibitor.
- Cardiac function, hypertrophy, fibrosis, apoptosis, and angiogenesis were assessed.
Main Results:
- HDAC inhibition significantly improved cardiac function in diabetic mice.
- Treatment attenuated cardiac hypertrophy, interstitial fibrosis, and apoptosis.
- HDAC inhibition increased angiogenesis, glucose transporter expression, and antioxidant levels.
Conclusions:
- HDAC inhibition is a promising therapeutic strategy for diabetic cardiomyopathy.
- It plays a critical role in improving cardiac function and suppressing myocardial remodeling.
Background:
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.
Methods:
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.
Results:
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.
Conclusion:
HDAC inhibition plays a critical role in improving cardiac function and suppressing myocardial remodeling in diabetic heart.
