Oxidative Medicine and Cellular Longevity

Cell Death and Oxidative Stress in Inflammation-associated Damage and Diseases


Publishing date
01 Jul 2023
Status
Closed
Submission deadline
03 Mar 2023

Lead Editor

1National Cheng Kung University, Taiwan

2Roswell Park Cancer Institute, Buffalo, USA

3China Medical University, Taiwan

4Taipei Medical University, Taipei, Taiwan

This issue is now closed for submissions.

Cell Death and Oxidative Stress in Inflammation-associated Damage and Diseases

This issue is now closed for submissions.

Description

Cell death mechanisms are studied across a broad spectrum of models of oxidative stress, including hydrogen peroxide, endotoxin-induced inflammation, nitric oxide and derivatives, ultraviolet, photodynamic therapy, ionizing radiation and cigarette smoke. Reactive oxygen or nitrogen species (ROS/RNS) generated endogenously or in response to environmental stress or pollutants have long been implicated in tissue injury in a variety of disease states. Under some pathological conditions such as traumatic injury, hypoxia, and ischemia/reperfusion, the excessive ROS accumulation could break cellular homeostasis, resulting in oxidative stress and mitochondrial dysfunction. In recent years, many types of programmed cell death, including apoptosis, autophagy, necroptosis, pyroptosis, ferroptosis, and oxytosis, have received a lot of attention in disease research. There are a lot of published articles describing the relationship between cell death and oxidative stress in inflammation-associated damage and diseases. ROS accumulation can trigger many cellular stress responses, including DNA damage responses and other signal transduction-related responses. For instance, ROS-mediated DNA damage activates the ATM/ATR-p53 pathway, resulting in cellular senescence or cell death. In addition, oxidative stress could promote the formation of autophagy.

However, the matter of whether autophagy is protective or cytotoxic for anticancer treatment in cancer cells is an area of active investigation. In addition, the current interest in the linkage of oxidative stress to inflammation and inflammatory responses is adding a new perspective. Therefore, a better understanding of cell death and oxidative stress to find new therapeutic or preventive strategies for various diseases including cancer would be beneficial.

The aim of this Special Issue is to provide a broad and updated overview of the relationship between various cell death and oxidative stress in inflammation-associated damage and diseases. Furthermore, this Special Issue will focus on the potential impact of environmental pollutants on cell death and oxidative stress and strategies for their prevention and therapy. Studies on oxidative stress-induced tissue injury and cell death in chronic inflammation- and fibrosis-related diseases are also encouraged. Original research and review articles are welcome.

Potential topics include but are not limited to the following:

  • Molecular mechanism of the inflammasomes activation and pyroptosis
  • Exploring novel molecular mechanisms and crosstalk between cell death and oxidative stress
  • Oxidative stress and cellular senescence in fibrotic diseases or cancer
  • Potential impact of environmental pollutants on cell death and oxidative stress
  • Apoptosis and oxidative stress in inflammation-associated damage and diseases including cancer
  • Oxidative stress, redox signaling, and autophagy
  • Role of necroptosis in chronic inflammation and fibrosis
  • Crosstalk between endoplasmic reticulum (ER) stress, oxidative stress, and inflammation
  • Iron homeostasis and iron-regulated ROS in ferroptotic cell death, senescence and human diseases
  • Crosstalk between oxidative stress and oxytosis in inflammation-associated damage and diseases
  • Therapeutic possibilities of antioxidants on the oxidative stress-induced diseases, tissue injury, and cell death
Oxidative Medicine and Cellular Longevity
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