Oxidative Medicine and Cellular Longevity

Mechanisms and Therapies of Oxidative Stress-Mediated Cell Death in Ischemia Reperfusion Injury 2021


Publishing date
01 Sep 2021
Status
Closed
Submission deadline
30 Apr 2021

Guest Editors

1Massachusetts General Hospital, Boston, USA

2Shenzhen University, Shenzhen, China

This issue is now closed for submissions.
More articles will be published in the near future.

Mechanisms and Therapies of Oxidative Stress-Mediated Cell Death in Ischemia Reperfusion Injury 2021

This issue is now closed for submissions.
More articles will be published in the near future.

Description

Oxidative stress, initiated by burst production of reactive oxygen species (ROS), plays an important role in ischemia reperfusion injury by affecting cell death processes (apoptosis, necrosis, and autophagy). 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 pro-death signals that lead to cell death while autophagy is a predominantly cytoprotective process serving as a pro-survival function in ischemia reperfusion injury.

During ischemia reperfusion, oxidative stress, by inducing apoptosis and necroptosis on the 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 targeting these three types of cell death in ischemia reperfusion injury are lacking.

We invite investigators to contribute original research articles as well as review articles that will stimulate 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)
  • The 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 signalling pathways targeting cell death (apoptosis, necroptosis, and autophagy) that contribute to cellular repair 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 2021
  • - Article ID 9929687
  • - Review Article

Ferroptosis: Opportunities and Challenges in Myocardial Ischemia-Reperfusion Injury

Wei-kun Zhao | Yao Zhou | ... | Qi Wu
  • Special Issue
  • - Volume 2021
  • - Article ID 6256399
  • - Research Article

PER2 Regulates Reactive Oxygen Species Production in the Circadian Susceptibility to Ischemia/Reperfusion Injury in the Heart

Yaqian Weng | Hui Li | ... | Le Li
  • Special Issue
  • - Volume 2021
  • - Article ID 2514947
  • - Research Article

miRNA-27a Transcription Activated by c-Fos Regulates Myocardial Ischemia-Reperfusion Injury by Targeting ATAD3a

Yandong Bao | Ying Qiao | ... | Dalin Jia
  • Special Issue
  • - Volume 2021
  • - Article ID 5543340
  • - Research Article

Computational and Preclinical Evidence of Anti-ischemic Properties of L-Carnitine-Rich Supplement via Stimulation of Anti-inflammatory and Antioxidant Events in Testicular Torsed Rats

Janet Olayemi Olugbodi | Keren Samaila | ... | Gaber El-Saber Batiha
  • Special Issue
  • - Volume 2021
  • - Article ID 8377362
  • - Review Article

Baicalein, Baicalin, and Wogonin: Protective Effects against Ischemia-Induced Neurodegeneration in the Brain and Retina

Li Pan | Kin-Sang Cho | ... | Chi-Wai Do
  • Special Issue
  • - Volume 2021
  • - Article ID 5524705
  • - Research Article

Supplemental N-3 Polyunsaturated Fatty Acids Limit A1-Specific Astrocyte Polarization via Attenuating Mitochondrial Dysfunction in Ischemic Stroke in Mice

Jun Cao | Lijun Dong | ... | Tao Tao
  • Special Issue
  • - Volume 2021
  • - Article ID 9985701
  • - Review Article

Cellular Signal Transduction Pathways Involved in Acute Lung Injury Induced by Intestinal Ischemia-Reperfusion

Guangyao Li | Yingyi Zhang | Zhe Fan
  • Special Issue
  • - Volume 2021
  • - Article ID 6657529
  • - Research Article

Inactivation of TOPK Caused by Hyperglycemia Blocks Diabetic Heart Sensitivity to Sevoflurane Postconditioning by Impairing the PTEN/PI3K/Akt Signaling

Sumin Gao | Rong Wang | ... | Tingting Wang
Oxidative Medicine and Cellular Longevity
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