The Role of DNA Methylation in Stroke Recovery.
Dong-Hee ChoiIn-Ae ChoiJong Min LeePublished in: International journal of molecular sciences (2022)
Epigenetic alterations affect the onset of ischemic stroke, brain injury after stroke, and mechanisms of poststroke recovery. In particular, DNA methylation can be dynamically altered by maintaining normal brain function or inducing abnormal brain damage. DNA methylation is regulated by DNA methyltransferase (DNMT), which promotes methylation, DNA demethylase, which removes methyl groups, and methyl-cytosine-phosphate-guanine-binding domain (MBD) protein, which binds methylated DNA and inhibits gene expression. Investigating the effects of modulating DNMT, TET, and MBD protein expression on neuronal cell death and neurorepair in ischemic stroke and elucidating the underlying mechanisms can facilitate the formulation of therapeutic strategies for neuroprotection and promotion of neuronal recovery after stroke. In this review, we summarize the role of DNA methylation in neuroprotection and neuronal recovery after stroke according to the current knowledge regarding the effects of DNA methylation on excitotoxicity, oxidative stress, apoptosis, neuroinflammation, and recovery after ischemic stroke. This review of the literature regarding the role of DNA methylation in neuroprotection and functional recovery after stroke may contribute to the development and application of novel therapeutic strategies for stroke.
Keyphrases
- dna methylation
- cerebral ischemia
- brain injury
- gene expression
- subarachnoid hemorrhage
- genome wide
- oxidative stress
- atrial fibrillation
- cell death
- blood brain barrier
- circulating tumor
- cell free
- healthcare
- drug delivery
- white matter
- endoplasmic reticulum stress
- signaling pathway
- dna damage
- inflammatory response
- small molecule
- cell proliferation
- protein protein
- transcription factor
- resting state
- circulating tumor cells
- lps induced