Pharmacologic Strategies to Target Oxidative Stress in Heart Failure

Ahmed, Zain; Tang, W.H. Wilson

doi:10.1007/s11897-011-0081-5

Cited by 27 publications

(24 citation statements)

References 84 publications

(64 reference statements)

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“…Endothelial dysfunction and failed angiogenesis occurs in patients with heart infarction [18,19]. NO has been extensively studied regarding its proangiogenic roles in endothelial homeostasis, migration, proliferation, and tube formation[20].…”

Section: Discussionmentioning

confidence: 99%

Deterioration of Cardiac Function After Acute Myocardial Infarction is Prevented by Transplantation of Modified Endothelial Progenitor Cells Overexpressing Endothelial NO Synthases

Chen

Zhao

et al. 2013

Cell Physiol Biochem

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Background/Aims: Stem cell transplantation and gene therapies have been shown to attenuate myocardial dysfunction after myocardial infarction (AMI) in different acute and chronic animal models. The aim of this study was to assess the potential therapeutic efficacy of endothelial NO synthases (eNOS)-expressing endothelial progenitor cells (EPCs) on infarcted hearts. Methods: Lentiviral eNOS-infected EPCs were injected after 1 h of ligation of the left anterior descending artery (LAD). The pro-inflammatory cytokines TNF-α and IL-1β levels in cardiac tissue were measured by ELISA at 3 days after transplantation. 28 days post AMI (before sacrifice), Left ventricular function of each group was determined by echocardiography and pressure-volume system. Cardiac tissues were analyzed with hematoxylin and eosin (H&E) staining and immunohistochemisty. eNOS expression in cardiac tissues was detected by western blot, and NO production of cardiac tissues was determined using an NO assay kit. Results: TNF-α and IL-1β levels in cardiac tissue were decreased significantly at 3 days after transplantation of lentiviral with eNOS infected EPCs compared to medium control, eNOS lentiviral vector and normal EPCs. At the 28 day after AMI, echocardiography and hemodynamic measurements, and isolated heart studies showed great therapeutic efficacy in improvement of cardiac function, reduction of infarcted size and improvement of vascular densities in the peri-infarct region after intramyocardial application of lentiviral eNOS-infected EPCs compared to medium control, eNOS lentiviral vector and normal EPCs. The eNOS over-expression in cardiac tissue was observed in the eNOS-EPCs and eNOS lentiviral vector group, and NO levels were increased significantly in the eNOS-EPCs and eNOS lentiviral vector group compared to the other three groups (sham operated group, transplantation of medium or EPCs group). Conclusion: EPCs can be an attractive vehicle for the exogenous eNOS expression into heart after infarction, which is beneficial to prevent deterioration and promote restoration of cardiac function after AMI by improving angiogenesis.

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Section: Discussionmentioning

confidence: 99%

Deterioration of Cardiac Function After Acute Myocardial Infarction is Prevented by Transplantation of Modified Endothelial Progenitor Cells Overexpressing Endothelial NO Synthases

Chen

Zhao

et al. 2013

Cell Physiol Biochem

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“…109, 110 Many different interventions have been tried including alpha tocopherol, ascorbic acid, and allopurinol to target xanthine oxidase. The results of clinical trials have been mixed with no convincing evidence that outcomes are improved in heart failure.…”

Section: Ss-31 and Mitochondrial Rosmentioning

confidence: 99%

“…The results of clinical trials have been mixed with no convincing evidence that outcomes are improved in heart failure. 109 A likely issue is the systemic nature of the treatments, when targeted reduction in ROS in cardiac cells is needed. Thus, even though there is substantial evidence that an increase in ROS is an important factor in heart failure, disappointingly, treatment strategies to date have been inconclusive to ineffective.…”

Section: Ss-31 and Mitochondrial Rosmentioning

confidence: 99%

Heart Failure and Mitochondrial Dysfunction

Knowlton

Chen

Malik

2014

Journal of Cardiovascular Pharmacology

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The treatment of heart failure has evolved during the last thirty years with recognition of neurohormonal activation and the effectiveness of its inhibition in improving quality of life and survival. Over the last twenty years there has been a revolution in the investigation of the mitochondrion with the development of new techniques and the finding that mitochondria are connected in networks and undergo constant division (fission) and fusion, even in cardiac myocytes. This has led to new molecular and cellular discoveries in heart failure, which offer the potential for the development of new molecular-based therapies. Reactive oxygen species (ROS) are an important cause of mitochondrial and cellular injury in heart failure, but there are other abnormalities, such as depressed mitochondrial fusion, that may eventually become targets of at least episodic treatment. The overall need for mitochondrial fission/fusion balance may preclude sustained change in either fission or fusion. In this review we will discuss current heart failure therapy and its impact on the mitochondria. In addition we will review some of the new drug targets under development. There is potential for effective, novel therapies for heart failure to arise from new molecular understanding.

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“…Oxidative stress is due to metabolic function degradation causing reactive oxygen species (ROS) accumulation (Ahmed and Tang 2012). This long-term oxidative stress is usually accompanied by inflammation in the elderly.…”

Section: Introductionmentioning

confidence: 99%

Resveratrol enhanced FOXO3 phosphorylation via synergetic activation of SIRT1 and PI3K/Akt signaling to improve the effects of exercise in elderly rat hearts

Lin

Wei³

et al. 2014

AGE

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Exercise training is considered a benefit to heart function, but the benefit in aging hearts remains unknown. Activation of the PI3K-Akt survival pathway and suppression of Fas/FADD/caspase-8 apoptotic signaling by exercise training in hearts from young subjects have been described in our previous studies. However, the mechanisms are still unclear and need to be explored in aging hearts. Thus, 18-month-old rats were used as a model and underwent swimming exercise training, resveratrol treatment (15 mg/kg/day), or exercise training with resveratrol treatment for 1 month. The results showed that heart function in each group improved. AGE (2014) 36:9705

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Pharmacologic Strategies to Target Oxidative Stress in Heart Failure

Cited by 27 publications

References 84 publications

Deterioration of Cardiac Function After Acute Myocardial Infarction is Prevented by Transplantation of Modified Endothelial Progenitor Cells Overexpressing Endothelial NO Synthases

Deterioration of Cardiac Function After Acute Myocardial Infarction is Prevented by Transplantation of Modified Endothelial Progenitor Cells Overexpressing Endothelial NO Synthases

Heart Failure and Mitochondrial Dysfunction

Resveratrol enhanced FOXO3 phosphorylation via synergetic activation of SIRT1 and PI3K/Akt signaling to improve the effects of exercise in elderly rat hearts

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