Crossroad Between Oxidative Stress and DNA Damage and Repair in Stroke

Dear Colleagues,

The topic “Crossroad Between Oxidative Stress and DNA Damage and Repair in Stroke” explores the intricate relationship between oxidative stress and DNA damage in the context of stroke and the cellular repair mechanisms involved. Stroke, particularly ischemic stroke, leads to a cascade of events that involve a loss of oxygen and nutrients to brain tissue, resulting in cellular damage. One of the primary consequences of this damage is the generation of reactive oxygen species (ROS) and other free radicals, which induce oxidative stress. Oxidative stress further exacerbates cellular injury by damaging critical macromolecules, including lipids, proteins, and DNA.

Key Areas to Cover: overview of stroke and its mechanisms: pathophysiology of stroke, including ischemic and hemorrhagic types. How lack of oxygen (ischemia) induces cellular stress and damage. Oxidative stress in stroke: the role of reactive oxygen species (ROS) and reactive nitrogen species (RNS) in stroke-induced damage. Mechanisms through which oxidative stress contributes to neuronal death, inflammation, and tissue injury. The impact of oxidative stress on brain cells, including neurons and glial cells. DNA damage in stroke: how oxidative stress leads to DNA damage, such as single-strand breaks, double-strand breaks, and base modifications. The relationship between oxidative DNA damage and neuronal death following stroke. DNA repair mechanisms in stroke: DNA repair pathways activated in response to oxidative DNA damage, such as base excision repair (BER), nucleotide excision repair (NER), and double-strand break repair mechanisms. The role of key repair enzymes, including PARP1, DNA ligases, and others, in maintaining cellular integrity. How these repair mechanisms might be dysregulated in stroke and contribute to cell survival or death. Molecular pathways connecting oxidative stress and DNA repair: crosstalk between oxidative stress signaling pathways and DNA repair pathways. The role of transcription factors, such as NF-κB, p53, and others, in regulating both oxidative stress responses and DNA damage repair mechanisms. Potential therapeutic strategies: strategies targeting oxidative stress, such as antioxidants, and their potential to reduce stroke damage. Developing drugs that enhance DNA repair mechanisms or modulate the DNA damage response to protect brain cells post-stroke. Clinical implications and future directions: Current research into biomarkers for oxidative stress and DNA damage following stroke. Challenges in translating oxidative stress and DNA repair findings into therapeutic options. Potential for clinical trials involving oxidative stress modulation or DNA repair enhancement in stroke patients.

Type of Submissions Expected:

• Review Articles: Comprehensive reviews on the current understanding of the relationship between oxidative stress and DNA damage/repair in stroke, summarizing the latest findings.
• Original Research Articles: Experimental studies that explore the mechanisms of oxidative stress and DNA repair in stroke models, including in vitro and in vivo work.
• Opinion Articles: Perspectives on potential therapeutic strategies to mitigate oxidative stress and enhance DNA repair after stroke. This area covers a multidisciplinary approach, integrating molecular biology, neuroscience, pharmacology, and clinical medicine.

The research could lead to developing more targeted therapeutic interventions aimed at reducing stroke-induced brain damage and improving patient outcomes.

Dr. William James Antonisamy
Dr. Zahoor Shah
Guest Editors

Dr. Moorthi Ponnusamy
Guest Editor Assistant

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• oxidative stress
• DNA damage
• DNA repair
• stroke
• ischemic stroke
• neuroinflamamtion
• intracranial hemorrhagic stroke
• neuronal death