Epigenetic Mechanisms in Ischemic Stroke
Summary
Ischaemic stroke triggers a complex cascade of molecular events in which epigenetic modifications play a central role by dynamically regulating gene expression without altering the underlying DNA sequence. Key mechanisms include DNA methylation, histone acetylation and methylation, and the actions of non-coding RNAs such as microRNAs and long non-coding RNAs. These modifications influence inflammatory responses, neuronal survival, blood–brain barrier integrity, angiogenesis and neural repair. Following an ischaemic insult, shifts in methylation patterns can suppress protective genes or activate proinflammatory pathways, while alterations in histone acetylation can open chromatin domains to allow transcription of repair factors. Non-coding RNAs further fine-tune the post-transcriptional landscape, modulating apoptosis, oxidative stress and neuroplasticity. Together, these epigenetic processes determine the severity of injury, the efficacy of endogenous repair and the potential for therapeutic intervention. Understanding these mechanisms offers new avenues for biomarker discovery and targeted therapies aimed at promoting neuroprotection and functional recovery on a global scale.
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Epigenetic Mechanisms in Ischemic Stroke publication trend
The graph below shows the total number of articles in epigenetic mechanisms in ischemic stroke across all publications each year (not limited to Nature Index journals).
Technical terms
DNA methylation: Addition of methyl groups to cytosine bases in DNA, often leading to gene repression.
Histone deacetylase (HDAC): Enzyme that removes acetyl groups from histone proteins, causing chromatin compaction and reduced transcription.
Blood–brain barrier (BBB): A selective endothelial interface that regulates passage of substances between the bloodstream and the brain.
Long non-coding RNA (lncRNA): RNA molecules longer than 200 nucleotides that do not code for proteins but modulate gene expression through diverse mechanisms.
References
- DNMT3A dysfunction promotes neuroinflammation and exacerbates acute ischemic stroke. MedComm (2024).
- Histone deacetylase inhibition by suberoylanilide hydroxamic acid during reperfusion promotes multifaceted brain and vascular protection in spontaneously hypertensive rats with transient ischaemic stroke. Biomedicine & Pharmacotherapy (2024).
- Epigenetics and stroke: role of DNA methylation and effect of aging on blood–brain barrier recovery. Fluids and Barriers of the CNS (2023).
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