Testosterone improves cardiac function and alters angiotensin II receptors in isoproterenol-induced heart failure

Kang, Ningning; Fu, Lu; Xu, Jing; Han, Ying; Cao, Junxian; Sun, Jing; Zheng, Min

doi:10.1016/j.acvd.2011.12.002

Cited by 40 publications

(32 citation statements)

References 29 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…LV hemodynamics were evaluated as described previously [23]. Rats were anesthetized with 10 % chloral hydrate (3 ml/kg, peritoneal injection), the trachea was exposed, and the animal ventilator (HX-300, TME Technology Co., Ltd., China) was connected.…”

Section: Evaluation Of the Effects Of Afgf Treatment On Cardiac Functmentioning

confidence: 99%

Advanced Interfere Treatment of Diabetic Cardiomyopathy Rats by aFGF-Loaded Heparin-Modified Microbubbles and UTMD Technique

Zhang

Shen³

et al. 2016

Cardiovasc Drugs Ther

View full text Add to dashboard Cite

This study aims to investigate the preclinical performance and mechanism of a novel strategy of aFGF-loaded heparin-modified microbubbles (aFGF-HMB) combined with ultrasound-targeted microbubble destruction (UTMD) technique for diabetic cardiomyopathy (DCM) prevention. Type 1 diabetic rats were induced by streptozotocin. Twelve weeks after intervention, indexes from transthoracic echocardiography and cardiac catheterization showed that the left ventricular function in the aFGF-HMB/UTMD group was significantly improved compared with diabetes control (DM). From Picrosirius Red staining and TUNEL staining, the aFGF-HMB/UTMD group showed significant difference from the other groups. The cardiac collagen volume fraction (CVF) and myocardial cell apoptosis index (AI) in aFGF-HMB/UTMD group decreased to 7.2 % and 7.11 % respectively, compared with the DM group (CVF = 24.5 % and AI =20.3 % respectively). The results of myocardial microvascular density (MCD) also proved the strongest inhibition of aFGF-HMB/UTMD group on DCM progress. CD31 staining of aFGF-HMB/UTMD group reached 22 n/hrp, much higher than that of DM group (9 n/hrp). These results confirmed that the abnormalities including left ventricular dysfunction, myocardial fibrosis, cardiomyocytes apoptosis and microvascular rarefaction could be suppressed by twice weekly aFGF treatments for 12 consecutive weeks (free aFGF or aFGF-HMB+/-UTMD), with the strongest improvements observed in the aFGF-HMB/UTMD group (P < 0.05 vs free aFGF or aFGF-HMB). Western blot analyses of heart tissue further revealed the highest aFGF, anti-apoptosis protein (Bcl-2), VEGF-C, pAkt, pFoxo-3a levels and strongest reduction in pro-apoptosis proteins (Bax) level in aFGF-HMB/UTMD group. Overall, aFGF-HMB combined with UTMD technique might be developed as an effective strategy to prevent DCM in future clinical therapy.

show abstract

Section: Evaluation Of the Effects Of Afgf Treatment On Cardiac Functmentioning

confidence: 99%

Advanced Interfere Treatment of Diabetic Cardiomyopathy Rats by aFGF-Loaded Heparin-Modified Microbubbles and UTMD Technique

Zhang

Shen³

et al. 2016

Cardiovasc Drugs Ther

View full text Add to dashboard Cite

show abstract

“…Both obesity-related insulin resistance and testosterone deprivation are known to increase the risk of cardiovascular disease [1], and in both human [2] and animal studies have been shown to be associated with left-ventricular (LV) dysfunction and cardiac autonomic imbalance [3-5]. Previous reports suggested that these adverse cardiac effects are due to mitochondrial dysfunction [4, 6].…”

Section: Introductionmentioning

confidence: 99%

Testosterone Deprivation Aggravates Left-Ventricular Dysfunction in Male Obese Insulin-Resistant Rats via Impairing Cardiac Mitochondrial Function and Dynamics Proteins

et al. 2018

View full text Add to dashboard Cite

Background: We have previously reported that testosterone deprivation at a very young age accelerated, but did not aggravate, left-ventricular (LV) dysfunction in obese insulin-resistant rats. However, the effects of testosterone deprivation during adulthood on LV function in obese insulin-resistant rats remains unclear. We hypothesized that testosterone deprivation aggravates LV dysfunction and cardiac autonomic imbalance via the impairment of cardiac mitochondrial function and dynamics proteins, a reduction in insulin receptor function, and an increase in apoptosis in obese insulin-resistant rats. Methods: Male rats were fed on either a normal diet (ND) or a high-fat diet (HFD) for 12 weeks. They were then subdivided into 2 groups: sham operation (NDS, HFS) and orchiectomy (NDO, HFO). Metabolic parameters, blood pressure, heart rate variability (HRV), and LV function were determined at baseline and before and after orchiectomy. Mitochondrial function and dynamics proteins, insulin signaling, and apoptosis were determined 12 weeks postoperatively. Results: HFS rats exhibited obese insulin resistance, depressed HRV, and LV dysfunction. In HFO rats, systolic blood pressure was increased with more excessive depression of HRV and increased LV dysfunction, compared with HFS rats. These adverse cardiac effects were consistent with markedly increased mitochondrial dysfunction, reduced mitochondrial complex I and III proteins, reduced mitochondrial fusion proteins, and increased apoptosis, compared with HFS rats. However, testosterone deprivation did not lead to any alteration in the insulin-resistant condition in HFO rats, compared with HFS rats. Conclusion: We concluded that testosterone deprivation during adulthood aggravated the impairment of mitochondrial function, mitochondrial respiratory complex, mitochondrial dynamics proteins, and apoptosis, leading to LV dysfunction in obese insulin-resistant rats.

show abstract

“…Exercise capacity is highly correlated with myocardial diastolic function [11], and myocardial fibrosis is highly associated with diastolic dysfunction in patients with heart failure [12]. Physiological level of testosterone has been proven to ameliorate cardiac dysfunction and to attenuate myocardial fibrosis [13]. Accordingly, testosterone may improve exercise capacity in patients with heart failure by decreasing myocardial fibrosis at least in part.…”

mentioning

confidence: 98%

Reply to the letter “Androgens in cardiac fibrosis and other cardiovascular mechanisms”

Chung

Kao

et al. 2015

International Journal of Cardiology

View full text Add to dashboard Cite

Testosterone improves cardiac function and alters angiotensin II receptors in isoproterenol-induced heart failure

Abstract: These data suggest that androgen therapy could play an important role in pathophysiological changes in heart failure and have beneficial effects for its treatment.

Cited by 40 publications

References 29 publications

Advanced Interfere Treatment of Diabetic Cardiomyopathy Rats by aFGF-Loaded Heparin-Modified Microbubbles and UTMD Technique

Advanced Interfere Treatment of Diabetic Cardiomyopathy Rats by aFGF-Loaded Heparin-Modified Microbubbles and UTMD Technique

Testosterone Deprivation Aggravates Left-Ventricular Dysfunction in Male Obese Insulin-Resistant Rats via Impairing Cardiac Mitochondrial Function and Dynamics Proteins

Reply to the letter “Androgens in cardiac fibrosis and other cardiovascular mechanisms”

Contact Info

Product

Resources

About