Oxidative stress and DNA damage after cerebral ischemia: Potential therapeutic targets to preserve the genome and improve stroke recovery.

Oxidative stress and DNA damage after cerebral ischemia: Potential therapeutic targets to preserve the genome and improve stroke recovery. Neuropharmacology. 2017 Nov 08;: Authors: Li P, Anne Stetler R, Leak RK, Shi Y, Li Y, Yu W, Bennett MVL, Chen J Abstract The past two decades have witnessed remarkable advances in oxidative stress research, particularly in the context of ischemic brain injury. Oxidative stress in ischemic tissues compromises the integrity of the genome, resulting in DNA lesions, cell death in neurons, glial cells, and vascular cells, and impairments in neurological recovery after stroke. As DNA is particularly vulnerable to oxidative attack, cells have evolved the ability to induce multiple DNA repair mechanisms, including base excision repair (BER), nucleotide excision repair (NER) and non-homogenous endpoint jointing (NHEJ). Defective DNA repair is tightly correlated with worse neurological outcomes after stroke, whereas upregulation of DNA repair enzymes, such as APE1, OGG1, and XRCC1, improves long-term functional recovery following stroke. Indeed, DNA damage and repair are now known to play critical roles in fundamental aspects of stroke recovery, such as neurogenesis, white matter recovery, and neurovascular unit remodeling. Several DNA repair enzymes are essential for comprehensive neural repair mechanisms after stroke, including PolĪ² and NEIL3 for neurogenesis, APE1 for white matter repair, Gadd45b for ax...
Source: Neuropharmacology - Category: Drugs & Pharmacology Authors: Tags: Neuropharmacology Source Type: research