Autophagy-Mediated Cellular Oxidative Stress Regulations
A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Health Outcomes of Antioxidants and Oxidative Stress".
Deadline for manuscript submissions: closed (15 March 2023) | Viewed by 11685
Special Issue Editor
Special Issue Information
Dear Colleagues,
Autophagy is a dynamic catabolic process playing a central role in maintaining cellular homeostasis. Through the autophagic pathway, cells degrade and recycle unnecessary or dysfunctional cytoplasmic components, including proteins and damaged organelles. Autophagy can be activated in response to diverse stressors such as nutrient deprivation, hypoxia, drugs and virus-mediated infections. A growing amount of evidence in recent years indicates for autophagy a role as a crucial mediator in the regulation of oxidative stress response. Oxidative stress is the result of the activity of both reactive oxygen species (ROS) and reactive nitrogen species (RNS) mainly produced through oxygen metabolism in mitochondria. ROS/RNS at physiological levels act as signalling molecules that regulate numerous cellular conditions whereas an excessive production can eventually cause cell death and give rise to a variety of diseases. In addition, high levels of oxidative stress can dysregulate autophagy favouring the accumulation of harmful aggregates. Thus, a complex interplay exists between these two processes that still remains unclear.
This Special Issue aims to collect research articles and reviews that deeply dissect and try to unravel the exact mechanisms that regulate the relationship between autophagy and oxidative stress, highlighting the role of mediators of this crosstalk and the correlations with disorders and aging.
Dr. Valentina Cecarini
Guest Editor
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Keywords
- oxidative stress
- reactive oxygen species
- autophagy
- aging
- proteolysis
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