Oxidative Stress and Cell Senescence Process—2nd Edition

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 (30 September 2023) | Viewed by 1275

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Guest Editor
Department of Molecular Medicine and Medical Biotechnologies, University of Naples Federico II, 80131 Naples, Italy
Interests: oxidative stress; cellular senescence; transcription factors; non coding RNAs; chromatin remodeling factors
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Special Issue Information

Dear Colleagues,

Oxidative stress occurs when the production of reactive oxygen species/reactive nitrogen species (ROS/RNS) overwhelms the endogenous antioxidant defenses. Under physiological conditions, the amounts of ROS/RNS are finely controlled and “Redox Homeostasis” involves molecular pathways that constantly provide cell equilibrium between their production and clearance/inactivation. During recent decades, overwhelming research evidence shows the central role of oxidative stress in a number of physio-pathological events, including the telomere-independent cell senescence process. In early life, cell senescence represents a safety program to permanently arrest damaged cells, but it is a ruling contributor in aging and age-related diseases. For this reason, particular attention is given to strategies that can delay or counteract senescence induced by ROS/RNS deregulation, thus, improving healthy aging and mitigating age-related diseases.

The senescence process is sustained by a reprogrammed gene expression, involving transcriptional and post-transcriptional mechanisms, as well as epigenetic regulatory events. This Special Issue aims to describe the interplay between oxidative stress, non-coding RNAs (microRNAs, long-non-coding RNAs and circular RNAs) and the senescence process. In recent years, non-coding RNAs turned out to be important redox-sensitive players, acting as regulators in whole signaling networks that can either boost or delay cell senescence. Since their expression or activities can be affected by ROS/RNS levels, non-coding RNAs represent interesting molecules, and ongoing research in the oxidative stress field is focused on this topic. We invite the submission of research findings/reviews delineating activities of these molecules on redox-sensitive signaling linked to senescence. This will contribute toward the emerging evidence concerning the use of synthetic molecules for in vivo delivery or antioxidants supplementation with future therapeutic purposes.

Dr. Raffaella Faraonio
Guest Editor

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Keywords

  • oxidative stress
  • cellular senescence
  • non-coding RNAs
  • redox transcription factors
  • antioxidant

Published Papers (1 paper)

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Research

17 pages, 3558 KiB  
Article
Oxymatrine Improves Oxidative Stress-Induced Senescence in HT22 Cells and Mice via the Activation of AMP-Activated Protein Kinase
by Nagarajan Maharajan, Chang-Min Lee, Karthikeyan A. Vijayakumar and Gwang-Won Cho
Antioxidants 2023, 12(12), 2078; https://doi.org/10.3390/antiox12122078 - 06 Dec 2023
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Abstract
The accumulation of oxidative stress is one of the important factors causing cellular senescence. Oxymatrine (OM) is a natural quinolizidine alkaloid compound known for its antioxidant effects. This study aimed to investigate the anti-senescence potential of OM through oxidative stress-induced in vitro and [...] Read more.
The accumulation of oxidative stress is one of the important factors causing cellular senescence. Oxymatrine (OM) is a natural quinolizidine alkaloid compound known for its antioxidant effects. This study aimed to investigate the anti-senescence potential of OM through oxidative stress-induced in vitro and in vivo models. By treating 600 μM of H2O2 to the HT22 mouse hippocampal neuronal cell line and by administering 150 mg/kg D-galactose to mice, we generated oxidative stress-induced senescence models. After providing 1, 2, and 4 μg/mL of OM to the HT22 mouse cell line and by administering 50 mg/kg OM to mice, we evaluated the enhancing effects. We evaluated different senescence markers, AMPK activity, and autophagy, along with DCFH-DA detection reaction and behavioral tests. In HT22 cells, OM showed a protective effect. OM, by reducing ROS and increasing p-AMPK expression, could potentially reduce oxidative stress-induced senescence. In the D-Gal-induced senescence mouse model, both the brain and heart tissues recovered AMPK activity, resulting in reduced levels of senescence. In neural tissue, to assess neurological recovery, including anxiety symptoms and exploration, we used a behavioral test. We also found that OM decreased the expression level of receptors for advanced glycation end products (RAGE). In heart tissue, we could observe the restoration of AMPK activity, which also increased the activity of autophagy. The results of our study suggest that OM ameliorates oxidative stress-induced senescence through its antioxidant action by restoring AMPK activity. Full article
(This article belongs to the Special Issue Oxidative Stress and Cell Senescence Process—2nd Edition)
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