Oxidative Medicine and Cellular Longevity

Mechanism and Therapies of Oxidative Stress-Mediated Cell Death in Ischemia Reperfusion Injury


Status
Published

Lead Editor

1Harvard Medical School, Boston, USA

2University of Hong Kong, Pokfulam, Hong Kong

3Wright State University Boonshoft, Dayton, USA

4Memorial University of Newfoundland, St. John’s, Canada

5First Affiliated Hospital of Xinjiang Medical University, Xinjiang, China


Mechanism and Therapies of Oxidative Stress-Mediated Cell Death in Ischemia Reperfusion Injury

Description

Oxidative stress, initiated by burst production of reactive oxygen species (ROS), through inducing cell death (apoptosis, necrosis, and autophagy) plays important role in ischemia reperfusion injury. Apoptosis, autophagy, and the newly identified necroptosis are three major types of programmed cell death that participate in the pathogenesis of ischemia reperfusion injury, in which apoptosis and necroptosis function as prodeath signals that lead to cell death while autophagy is a predominant cytoprotective process serving as a prosurvival function in ischemia reperfusion injury. During ischemia reperfusion, oxidative stress by inducing apoptosis and necroptosis on one hand and by disrupting autophagy (imbalance of autophagosome formation and degradation) on the other hand jointly causes mitochondrial dysfunction and further enhances oxidative stress, resulting in cell death and organ/cellular injury. Thus, reducing oxidative stress to maintain the balance among apoptosis, necroptosis, and autophagy is of particular importance in the attenuation of ischemia reperfusion injury. However, the molecular mechanism governing oxidative stress-induced apoptosis, necroptosis, and autophagy is unclear and therapies that target these three types of cell death in combating ischemia reperfusion injury are lacking.

We invite investigators to contribute original research articles as well as review articles that will stimulate the continuing efforts to understand the molecular mechanism underlying oxidative stress-induced cell death (apoptosis, necroptosis, and autophagy) in ischemia reperfusion injury under normal and diseased conditions to develop strategies to treat these pathological conditions.

Potential topics include but are not limited to the following:

  • Roles of apoptosis, necroptosis, and autophagy in organ (heart, lung, brain, liver, kidney, and/or intestine) ischemia reperfusion injury under normal and diseased conditions (e.g., diabetes and aging)
  • Role of reactive oxygen species (ROS) in organ ischemia reperfusion injury under normal and diseased conditions and its interplay with apoptosis, necroptosis, and autophagy
  • Cellular protective signaling pathways targeting cell death (apoptosis, necroptosis, and autophagy) that contribute to cellular repairing during ischemia reperfusion injury and the potential interplay between these pathways
  • Cardioprotection in aged and/or functionally impaired hearts
  • Role of mitochondrial function in oxidative stress and inflammation-mediated remote organ injury during ischemia reperfusion
  • Recent advances in preventing ischemia-reperfusion injury with a focus on oxidative stress and cell death

Articles

  • Special Issue
  • - Volume 2018
  • - Article ID 2910643
  • - Editorial

Mechanism and Therapies of Oxidative Stress-Mediated Cell Death in Ischemia Reperfusion Injury

Haobo Li | Zhengyuan Xia | ... | Hong Zheng
  • Special Issue
  • - Volume 2018
  • - Article ID 9865495
  • - Research Article

Troxerutin Protects Kidney Tissue against BDE-47-Induced Inflammatory Damage through CXCR4-TXNIP/NLRP3 Signaling

Qun Shan | Gui-hong Zheng | ... | Yuan-Lin Zheng
  • Special Issue
  • - Volume 2018
  • - Article ID 6403861
  • - Research Article

Transduced PEP-1-Heme Oxygenase-1 Fusion Protein Attenuates Lung Injury in Septic Shock Rats

Xue-Tao Yan | Xiang-Hu He | ... | Jun-Jiao Tang
  • Special Issue
  • - Volume 2017
  • - Article ID 2490501
  • - Research Article

Roles of Endoplasmic Reticulum Stress in NECA-Induced Cardioprotection against Ischemia/Reperfusion Injury

Fengmei Xing | Hui Han | ... | Jinkun Xi
  • Special Issue
  • - Volume 2017
  • - Article ID 3861914
  • - Research Article

Pretreatment Donors after Circulatory Death with Simvastatin Alleviates Liver Ischemia Reperfusion Injury through a KLF2-Dependent Mechanism in Rat

Zhongzhong Liu | Xingjian Zhang | ... | Yanfeng Wang
  • Special Issue
  • - Volume 2017
  • - Article ID 6034692
  • - Research Article

Troxerutin Reduces Kidney Damage against BDE-47-Induced Apoptosis via Inhibiting NOX2 Activity and Increasing Nrf2 Activity

Qun Shan | Juan Zhuang | ... | Yuanlin Zheng
  • Special Issue
  • - Volume 2017
  • - Article ID 3542149
  • - Research Article

Inhibition of Caveolae Contributes to Propofol Preconditioning-Suppressed Microvesicles Release and Cell Injury by Hypoxia-Reoxygenation

Fan Deng | Shuang Wang | ... | Liangqing Zhang
  • Special Issue
  • - Volume 2017
  • - Article ID 9743280
  • - Research Article

NLRP3 Inflammasome Activation-Mediated Pyroptosis Aggravates Myocardial Ischemia/Reperfusion Injury in Diabetic Rats

Zhen Qiu | Shaoqing Lei | ... | Zhong-yuan Xia
  • Special Issue
  • - Volume 2017
  • - Article ID 3869561
  • - Research Article

Expression and Role of the Calcium-Sensing Receptor in Rat Peripheral Blood Polymorphonuclear Neutrophils

Tai-yu Zhai | Bao-hong Cui | ... | Yi-hua Sun
  • Special Issue
  • - Volume 2017
  • - Article ID 8326749
  • - Research Article

PPAR-γ Activation Prevents Septic Cardiac Dysfunction via Inhibition of Apoptosis and Necroptosis

Shiyan Peng | Junmei Xu | ... | Feng Xiao
Oxidative Medicine and Cellular Longevity
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Acceptance rate48%
Submission to final decision56 days
Acceptance to publication37 days
CiteScore7.900
Impact Factor6.543
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