Abstract
Cerebral ischemia is the second leading cause of death in the world and multimodal stroke therapy is needed. The ischemic stroke generally reduces the gene expression due to suppression of acetylation of histones H3 and H4. Histone deacetylases inhibitors have been shown to be effective in protecting the brain from ischemic damage. Histone deacetylases inhibitors induce neurogenesis and angiogenesis in damaged brain areas promoting functional recovery after cerebral ischemia. However, the role of different histone deacetylases isoforms in the survival and death of brain cells after stroke is still controversial. This review aims to analyze the data on the neuroprotective activity of nonspecific and selective histone deacetylase inhibitors in ischemic stroke.
Highlights
Cerebral ischemia is the second leading cause of death in the world and multimodal stroke therapy is needed
This review aims to analyze the data on the neuroprotective activity of nonspecific and selective histone deacetylase inhibitors in ischemic stroke
In the present review we focus on the role of non-mitochondrial SIRT1, SIRT2, and SIRT6 in the brain damage and recovery after ischemic stroke
Summary
Stroke is one of the leading causes of death in the world [1]. About 5 million people die every year. Stroke is a developing over time multi-stage process It starts from the primary minor changes and leads to the formation of a penumbra, death or restoration of its cells, and to the irreversible structural damage of brain tissue causing neurodegeneration. A huge number of pathophysiological and biochemical processes in intracellular and intercellular signaling, proteolysis, and regulation of the transcriptional activity of the genome are occurred in between these phases Each of these stages is the time point of possible application of anti-stroke drugs. Numerous studies searching targets for neuroprotection have highlighted the importance of multimodal stroke therapy An example of such a strategy, which has been shown to be effective in various models of ischemia, is the inhibition of histone deacetylases.
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
