scholarly journals Quantitative systems models illuminate arrhythmia mechanisms in heart failure: Role of the Na+ -Ca2+ -Ca2+ /calmodulin-dependent protein kinase II-reactive oxygen species feedback

2018 ◽  
Vol 11 (2) ◽  
pp. e1434 ◽  
Author(s):  
Stefano Morotti ◽  
Eleonora Grandi
Keyword(s):  
Heart Failure ◽  
Reactive Oxygen Species ◽  
Protein Kinase ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Dependent Protein Kinase ◽  
Arrhythmia Mechanisms ◽  
Dependent Protein ◽  
Systems Models

Reactive Oxygen Species Elicit Apoptosis by Concurrently Disrupting Topoisomerase II and DNA-Dependent Protein Kinase

2005 ◽  
Vol 68 (4) ◽  
pp. 983-994 ◽  
Author(s):  
Hua-Rui Lu ◽  
Hong Zhu ◽  
Min Huang ◽  
Yi Chen ◽  
Yu-Jun Cai ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Protein Kinase ◽  
Topoisomerase Ii ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Dependent Protein Kinase ◽  
Dependent Protein

The role of nitric oxide, reactive oxygen species, and protein kinase C in oxytocin-induced cardioprotection in ischemic rat heart

Peptides ◽  
2012 ◽  
Vol 37 (2) ◽  
pp. 314-319 ◽  
Author(s):  
Mahdieh Faghihi ◽  
Ali Mohammad Alizadeh ◽  
Vahid Khori ◽  
Mostafa Latifpour ◽  
Saeed Khodayari
Keyword(s):  
Nitric Oxide ◽  
Reactive Oxygen Species ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Rat Heart ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Kinase C

The role of reactive oxygen species in the hearts of dystrophin-deficient mdx mice

2007 ◽  
Vol 293 (3) ◽  
pp. H1969-H1977 ◽  
Author(s):  
Iwan A. Williams ◽  
David G. Allen
Keyword(s):  
Heart Failure ◽  
Reactive Oxygen Species ◽  
Oxidative Damage ◽  
Collagen Type ◽  
Reactive Oxygen ◽  
Mdx Mice ◽  
Oxygen Species ◽  
Collagen Type Iii ◽  
Fractional Shortening

Duchenne muscular dystrophy (DMD) is caused by deficiency of the cytoskeletal protein dystrophin. Oxidative stress is thought to contribute to the skeletal muscle damage in DMD; however, little is known about the role of oxidative damage in the pathogenesis of the heart failure that occurs in DMD patients. The dystrophin-deficient ( mdx) mouse is an animal model of DMD that also lacks dystrophin. The current study investigates the role of the antioxidant N-acetylcysteine (NAC) on mdx cardiomyocyte function, Ca2+ handling, and the cardiac inflammatory response. Treated mice received 1% NAC in their drinking water for 6 wk. NAC had no effect on wild-type (WT) mice. Immunohistochemistry experiments revealed that mdx mice had increased dihydroethidine (DHE) staining, an indicator of superoxide production; NAC-treatment reduced DHE staining in mdx hearts. NAC treatment attenuated abnormalities in mdx cardiomyocyte Ca2+ handling. Mdx cardiomyocytes had decreased fractional shortening and decreased Ca2+ sensitivity; NAC treatment returned mdx fractional shortening to WT values but did not affect the Ca2+ sensitivity. Immunohistochemistry experiments revealed that mdx hearts had increased levels of collagen type III and the macrophage-specific protein, CD68; NAC-treatment returned collagen type III and CD68 expression close to WT values. Finally, mdx hearts had increased NADPH oxidase activity, suggesting it could be a possible source of increased reactive oxygen species in mdx mice. This study is the first to demonstrate that oxidative damage may be involved in the pathogenesis of the heart failure that occurs in mdx mice. Therapies designed to reduce oxidative damage might be beneficial to DMD patients with heart failure.

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