Overexpression of glutathione peroxidase attenuates myocardial remodeling and preserves diastolic function in diabetic heart.

@article{Matsushima2006OverexpressionOG,
  title={Overexpression of glutathione peroxidase attenuates myocardial remodeling and preserves diastolic function in diabetic heart.},
  author={Shouji Matsushima and Shintaro Kinugawa and Tomomi Ide and Hidenori Matsusaka and Naoki Inoue and Yukihiro Ohta and Takashi Yokota and Kenji Sunagawa and Hiroyuki Tsutsui},
  journal={American journal of physiology. Heart and circulatory physiology},
  year={2006},
  volume={291 5},
  pages={
          H2237-45
        }
}
Oxidative stress plays an important role in the structural and functional abnormalities of diabetic heart. Glutathione peroxidase (GSHPx) is a critical antioxidant enzyme that removes H(2)O(2) in both the cytosol and mitochondia. We hypothesized that the overexpression of GSHPx gene could attenuate left ventricular (LV) remodeling in diabetes mellitus (DM). We induced DM by injection of streptozotocin (160 mg/kg ip) in male GSHPx transgenic mice (TG+DM) and nontransgenic wildtype littermates… 
View on PubMed
ajpheart.physiology.org
105 Citations
Background Citations
36
Methods Citations
3
Results Citations
3

105 Citations

Citation Type

Citation Type

Glutathione peroxidase 1 protects mitochondria against hypoxia/reoxygenation damage in mouse hearts
TLDR
The first report of the role of GPx1 in protecting cardiac mitochondria against reoxygenation damage in vivo is reported, which will help clarify the mechanisms of HR injury and will aid in the development of antioxidant therapies to prevent cardiac mitochondrial dysfunction associated with re Oxygenation.
Therapeutic potential of targeting oxidative stress in diabetic cardiomyopathy.
Cardiac fibrosis and dysfunction in experimental diabetic cardiomyopathy are ameliorated by alpha-lipoic acid
TLDR
It was shown that redox homeostasis was disturbed and MAPK signaling pathway components activated in STZ-induced DCM animals, while ALA treatment favorably shifted redoxHomeostasis and suppressed JNK and p38 MAPK activation.
Early loss of cardiac function in acute myocardial infarction is associated with redox imbalance.
TLDR
The data suggest that MI-induced cardiac dysfunction and impaired redox balance may be associated with the activation of counter-regulatory responses to maintain reduced H2O2 concentrations and, thereby, prevent further oxidative damage at this early time point.
Nrf2 Protects Against Maladaptive Cardiac Responses to Hemodynamic Stress
TLDR
These findings demonstrate that activation of Nrf2 provides a novel mechanism to protect the murine heart against pathological cardiac hypertrophy and heart failure via suppressing oxidative stress.
Significance of AT1 Receptor Independent Activation of Mineralocorticoid Receptor in Murine Diabetic Cardiomyopathy
TLDR
DM induced diastolic dysfunction was observed even in KO at 12 weeks, which was ameliorated by minelarocorticoid receptor antagonist, eplerenone, which suggests “aldosterone breakthrough” phenomenon.
Exercise enhances cardiac function by improving mitochondrial dysfunction and maintaining energy homoeostasis in the development of diabetic cardiomyopathy
TLDR
Protective effects of exercise on shifting energy metabolism from fatty acid oxidation to glucose oxidation in an established diabetic stage is demonstrated and suggest that exercise is effective at ameliorating diabetic cardiomyopathy by improving mitochondrial function and reducing metabolic disturbances.
Overexpression of human C-reactive protein exacerbates left ventricular remodeling in diabetic cardiomyopathy.
  • Y. Mano, T. Anzai, +8 authors K. Fukuda
  • Medicine, Biology
    Circulation journal : official journal of the Japanese Circulation Society
  • 2011
TLDR
Overexpression of human CRP exacerbates LV dysfunction and remodeling in diabetic cardiomyopathy, possibly through enhancement of the inflammation, renin-angiotensin system, and oxidative stress.
Oxidative stress and heart failure.
TLDR
Oxidative stress is involved in the pathophysiology of HF in the heart as well as in the skeletal muscle, and a better understanding of these mechanisms may enable the development of novel and effective therapeutic strategies against HF.
Zinc Prevents the Development of Diabetic Cardiomyopathy in db/db Mice
TLDR
It is suggested that zinc deficiency promotes the development and progression of DCM in T2DM db/ db mice, and the exacerbated effects by zinc deficiency on the heart of db/db mice may be related to further suppression of Nrf2 expression and function.
...
1
2
3
4
5
...

References

SHOWING 1-10 OF 37 REFERENCES
Antioxidant treatment attenuates hyperglycemia-induced cardiomyocyte death in rats.
Lipid peroxidation and activity of antioxidant enzymes in diabetic rats
TLDR
The findings suggest that oxidative stress occurs in diabetic state and that oxidative damage to tissues may be a contributory factor in complications associated with diabetes.
Treatment With Dimethylthiourea Prevents Left Ventricular Remodeling and Failure After Experimental Myocardial Infarction in Mice: Role of Oxidative Stress
TLDR
The attenuation of increased myocardial ROS and metalloproteinase activity with DMTU may contribute, at least in part, to its beneficial effects on LV remodeling and failure.
Endothelial relaxation is disturbed by oxidative stress in the diabetic rat heart: influence of tocopherol as antioxidant
TLDR
Findings demonstrate that oxidative stress may not only play a major role in the impairment of endothelium-dependent regulation of coronary flow, but also in the development of perivascular fibrosis and severe changes of the autonomic nerves and contractile system in myocardium.
Metallothionein prevents diabetes-induced deficits in cardiomyocytes by inhibiting reactive oxygen species production.
TLDR
The data show that diabetes induces damage at the level of individual myocyte, and diabetes increases ROS production via angiotensin II and flavoprotein enzyme-dependent pathways.
Abnormal cardiac function in the streptozotocin-diabetic rat. Changes in active and passive properties of the left ventricle.
TLDR
The hemodynamic and passive-elastic changes that occur in diabetic rats represent an early dilated cardiomyopathy which is reversible with insulin, and are concluded that the hemodynamics and Passive LV pressure-volume relationship was progressively shifted away from the pressure axis and the overall chamber stiffness constant was decreased.
Reduced activity of mtTFA decreases the transcription in mitochondria isolated from diabetic rat heart.
TLDR
A reduced binding activity of mtTFA to the D-loop region in the hearts of diabetic rats may contribute to the decreased mitochondrial protein synthesis.
Aminoguanidine prevents the decreased myocardial compliance produced by streptozotocin-induced diabetes mellitus in rats.
TLDR
It is demonstrated that diabetes mellitus can produce a stiff myocardium before the development of myocardial fibrosis and in these circumstances is associated with the formation of collagen AGEs.
Streptozotocin-induced hyperglycemia exacerbates left ventricular remodeling and failure after experimental myocardial infarction.
Inhibition of copper-zinc superoxide dismutase induces cell growth, hypertrophic phenotype, and apoptosis in neonatal rat cardiac myocytes in vitro.
TLDR
Increased intracellular superoxide resulting from inhibition of SOD causes activation of a growth program and apoptosis in cardiac myocytes, and these findings support a role for oxidative stress in the pathogenesis of myocardial remodeling and failure.
...
1
2
3
4
...