Reactive oxygen species-mediated cardiac-reperfusion injury: Mechanisms and therapies

Bagheri, Fariborz; Khori, Vahid; Alizadeh, Ali Mohammad; Khalighfard, Solmaz; Khodayari, Saeed; Khodayari, Hamid

doi:10.1016/j.lfs.2016.09.013

Cited by 100 publications

(83 citation statements)

References 143 publications

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“…ROS can be produced from several major sources, like cytochrome oxidase, unsaturated fatty acid oxidation, mitochondrial oxidation, and so on. And the most important ROS involved are O 2− , hydrogen peroxide (H 2 O 2 ), hypochlorous acid (HCLO), and OH − [21, 22]. When the balance between the production and scavenging of ROS is perturbed an irreversible damage to cells may occur, eventually leading to cell apoptosis and necrosis [23].…”

Section: Discussionmentioning

confidence: 99%

Amifostine Pretreatment Attenuates Myocardial Ischemia/Reperfusion Injury by Inhibiting Apoptosis and Oxidative Stress

Tao

Wang

et al. 2017

Oxidative Medicine and Cellular Longevity

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The present study was aimed at investigating the effect of amifostine on myocardial ischemia/reperfusion (I/R) injury of mice and H9c2 cells cultured with TBHP (tert-butyl hydroperoxide). The results showed that pretreatment with amifostine significantly attenuated cell apoptosis and death, accompanied by decreased reactive oxygen species (ROS) production and lower mitochondrial potential (ΔΨm). In vivo, amifostine pretreatment alleviated I/R injury and decreased myocardial apoptosis and infarct area, which was paralleled by increased superoxide dismutase (SOD) and reduced malondialdehyde (MDA) in myocardial tissues, increased Bcl2 expression, decreased Bax expression, lower cleaved caspase-3 level, fewer TUNEL positive cells, and fewer DHE-positive cells in heart. Our results indicate that amifostine pretreatment has a protective effect against myocardial I/R injury via scavenging ROS.

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Section: Discussionmentioning

confidence: 99%

Amifostine Pretreatment Attenuates Myocardial Ischemia/Reperfusion Injury by Inhibiting Apoptosis and Oxidative Stress

Tao

Wang

et al. 2017

Oxidative Medicine and Cellular Longevity

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“…When blood flow is restored after an ischaemic event, the myocardial tissue undergoes fast re‐oxygenation, which leads to mitochondrial electron transport chain dysfunction, oxidative stress and increased susceptibility to the opening of the mitochondrial permeability transition pore. These events lead to further increases in ROS production, enhanced leucocyte recruitment and vascular damage, although these are likely mediated by non‐neutrophil‐derived ROS …”

Section: Mechanisms Of Neutrophil‐induced Injurymentioning

confidence: 99%

“…These events lead to further increases in ROS production, enhanced leucocyte recruitment and vascular damage, although these are likely mediated by non-neutrophil-derived ROS. 47 Indirect evidence supporting the importance of neutrophil-derived ROS in vascular injury has been obtained from intravital imaging of neutrophils as they contact the vascular wall. 13,18 As neutrophils prepare to leave the circulation, they upregulate ICAM-1, and this ICAM-1 HI subset of neutrophils concomitantly produces higher levels of ROS.…”

Section: Reactive Oxygen Speciesmentioning

confidence: 99%

Neutrophils as effectors of vascular inflammation

Gómez-Moreno

Adrover

Hidalgo

2018

Eur J Clin Investigation

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Vascular inflammation underlies most forms of cardiovascular disease, which remains a prevalent cause of death among the global population. Advances in the biology of neutrophils, as well as insights into their dynamics in tissues, have revealed that these cells are prominent drivers of vascular inflammation though derailed activation within blood vessels. The development of powerful imaging techniques, as well as identification of cells and molecules that regulate their activation within vessels, including platelets and catecholamines, has been instrumental to better understand the mechanisms through which neutrophils protect or damage the organism. Other advances in our understanding of how these leucocytes exert detrimental functions on neighbouring cells, including the formation of DNA-based extracellular traps, constitute milestones in defining neutrophil-driven inflammation. Here, we review emerging mechanisms that regulate intravascular activation and effector functions of neutrophils, and discuss specific pathologies in which these processes are relevant. We argue that identification of pathways and mechanisms specifically engaged within the vasculature may provide effective therapies to treat this prevalent group of pathologies.

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“…Increasing in NO production is either increased by Endothelial Nitric Oxide Synthase (eNOS) enzymes [15][16][17] or reduced by Reactive Oxygen Species (ROS) [18]. Ischemic preconditioning causes ROS overproduction in the mitochondria under hypoxia [19,20]. However, the effect of hypoxia on Cx37, Cx40, Cx43, and Cx45 is unclear.…”

Section: Introductionmentioning

confidence: 99%

Characterization of Human Aortic Endothelial Cells, Endothelial Progenitor Cells, and Cardiomyocytes

Chen¹,

Kuo²

2017

J Tradi Med Clin Natur

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Despite advances in therapy, heart failure remains a significant disease burden, with poor outcomes, worldwide. Reactive Oxygen Species (ROS) damage cardiomyocytes. Endothelial progenitor cells promote the repair of the endothelium of arteries damaged by ROS. However, gene expression profiles of Human Aortic Endothelial Cells (HAECs), Endothelial Progenitor Cells (HEPCs), and Cardiomyocytes (HCMs) are unclear. In the present study, we determined the expression profiles of different genes in HAECs, HEPCs, and HCMs by performing quantitative PCR. Results showed that p53 and Cx37 were up-regulated, but VEGF, Cx43, and eNOS were down-regulated in HEPCs. Cx40 and eNOS were up-regulated in HAECs. Moreover, we determined the effect of hydrogen peroxide-derived ROS on HCMs. Results showed that Cx40, Cx45, VCAM-1, ICAM-1, p53, and p21 were up-regulated, but E-cadherin was down-regulated after high concentration of hydrogen peroxide treatment.

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Reactive oxygen species-mediated cardiac-reperfusion injury: Mechanisms and therapies

Cited by 100 publications

References 143 publications

Amifostine Pretreatment Attenuates Myocardial Ischemia/Reperfusion Injury by Inhibiting Apoptosis and Oxidative Stress

Amifostine Pretreatment Attenuates Myocardial Ischemia/Reperfusion Injury by Inhibiting Apoptosis and Oxidative Stress

Neutrophils as effectors of vascular inflammation

Characterization of Human Aortic Endothelial Cells, Endothelial Progenitor Cells, and Cardiomyocytes

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