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Updated: Apr 16, 2026
Post-Myocardial Infarction Heart Failure in Closed-chest Coronary Occlusion/Reperfusion Model in Göttingen Minipigs and Landrace Pigs
Published on: April 17, 2021
Testosterone suppresses ventricular remodeling and improves left ventricular function in rats following myocardial
Xiao-Fei Wang1, Xing-Qian Qu2, Tian-Tian Zhang1
1Department of Cardiology, Third People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 201900, P.R. China.
Insights
Testosterone treatment improved heart function and reduced cell death in male rats with congestive heart failure (CHF). This study found testosterone therapy suppressed ventricular remodeling and prevented mortality in a CHF rat model.
Area of Science:
- Cardiovascular Science
- Endocrinology
- Molecular Biology
Background:
- Congestive heart failure (CHF) is associated with low testosterone levels in men.
- Previous research indicates testosterone treatment can improve cardiac output and reduce vascular resistance.
- The precise impact of testosterone on heart function, cardiomyocyte apoptosis, and ventricular remodeling remains incompletely understood.
Purpose of the Study:
- To investigate the effects of testosterone on cardiac function, cardiomyocyte apoptosis, and ventricular remodeling in male rats following myocardial infarction.
- To assess the therapeutic potential of testosterone in a preclinical model of CHF.
Main Methods:
- A myocardial infarction model was established in male rats via coronary artery ligation.
- Rats with reduced left ventricular ejection fraction (LVEF ≤45%) were treated with low-dose, high-dose testosterone (TU), or placebo (PL) for 12 weeks.
- Quantitative polymerase chain reaction and immunofluorescence were used to analyze myocardial gene expression and caspase-3 levels.
Main Results:
- Testosterone treatment significantly improved LVEF compared to the placebo group.
- TU treatment reduced the mRNA expression of atrial natriuretic peptide, brain natriuretic peptide, matrix metalloproteinase-2, and sarcoendoplasmic reticulum Ca2+-ATPase 2a.
- TU treatment increased the mRNA expression of glycogen synthase kinase 3β and tissue inhibitor of metalloproteinase-2, and significantly reduced caspase-3 expression, indicating reduced apoptosis.
Conclusions:
- Testosterone therapy effectively suppressed ventricular remodeling and enhanced left ventricular function in a rat model of CHF.
- Testosterone treatment reduced cardiomyocyte apoptosis and improved survival rates in the CHF rat model.
- These findings suggest testosterone as a potential therapeutic agent for managing CHF in men.
Abstract:
Men with congestive heart failure (CHF) have relatively low testosterone levels. Several studies demonstrated that testosterone treatment increases cardiac output and reduces peripheral vascular resistance. However, the effects of testosterone on heart function, cardiomyocyte apoptosis and ventricular remodeling have not been fully elucidated. This study was conducted to investigate the effects of testosterone on heart function, cardiomyocyte apoptosis and ventricular remodeling in male rats post-myocardial infarction. A total of 86 male rats were randomly assigned to undergo ligation of the coronary artery (n=70) or pseudosurgery (n=16). After 6 weeks, a left ventricular ejection fraction (LVEF) of ≤45% was defined as a successful model of CHF. The model rats were randomly assigned to 3 groups, namely low-dose testosterone (TU), high-dose TU and placebo (PL) groups. After treatment for 12 weeks, the expression of several mRNA transcripts in myocardial tissue was measured by quantitative polymerase chain reaction. Immunofluorescence was used to measure myocardial caspase-3 expression. Compared to the PL group, LVEF was significantly improved in the TU treatment groups. Moreover, the mRNA expression of atrial natriuretic peptide, brain natriuretic peptide, matrix metalloproteinase-2 and sarcoendoplasmic reticulum Ca2+-ATPase 2a was significantly reduced, while the mRNA expression of glycogen synthase kinase 3β and tissue inhibitor of metalloproteinase-2 was markedly increased in the TU groups. TU treatment also significantly reduced caspase-3 expression. Therefore, different doses of TU suppressed ventricular remodeling and improved left ventricular function, reduced apoptosis and prevented mortality in a CHF rat model.
