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Published on: May 1, 2019
Histone deacetylases in stroke
1Taiwan International Graduate Program in Molecular Medicine, National Yang-Ming University and Academia Sinica, Taipei, Taiwan.
Abstract:
Stroke is the second leading cause of death and the leading cause of adult disability worldwide. Despite an impressive amount of neuroprotective agents that has been identified in experimental stroke, none of them proved efficient in clinical trials. There is a general consensus that an effective treatment requires the ability to interact with not one, but multiple pathophysiological cascades at different levels that induced by the insult - cocktail therapy. Luckily, recent progress in the field of epigenetics revealed that epigenetic modifications had influence on many known pathways involved in the complex course of ischemic disease development. The fact that epigenetic molecules, by altering transcriptional regulation, may simultaneously act on different levels of ischemic brain injury makes them promising candidates for clinical use. These modifications arise typically owing to deoxyribonucleic acid methylation and histone acetylation. The aim of this review is to give a comprehensive overview of current advances in stroke epigenetics, in particular, the physiological and pathological functions of the 11 classical histone deacetylases.
Insights
Epigenetics offers new hope for stroke treatment by targeting multiple injury pathways simultaneously. This review explores histone deacetylases as promising therapeutic targets for ischemic brain injury.
Area of Science:
- Neuroscience
- Molecular Biology
- Genetics
Background:
- Stroke is a leading cause of death and disability globally.
- Existing neuroprotective agents have shown limited success in clinical trials.
- Effective stroke treatment likely requires targeting multiple pathophysiological cascades.
Purpose of the Study:
- To provide a comprehensive overview of recent advances in stroke epigenetics.
- To highlight the potential of epigenetic modifications as therapeutic targets.
- To focus on the roles of histone deacetylases in ischemic brain injury.
Main Methods:
- Literature review of epigenetic mechanisms in stroke.
- Analysis of physiological and pathological functions of histone deacetylases.
- Exploration of transcriptional regulation in ischemic disease.
Main Results:
- Epigenetic modifications influence key pathways in ischemic disease development.
- Epigenetic molecules can act on multiple levels of brain injury simultaneously.
- Deoxyribonucleic acid methylation and histone acetylation are key epigenetic modifications.
Conclusions:
- Epigenetic strategies, particularly targeting histone deacetylases, show promise for stroke therapy.
- Modulating epigenetic mechanisms offers a potential 'cocktail therapy' approach.
- Further research into stroke epigenetics could lead to effective clinical treatments.
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