Glial Cells Response in Stroke.
Poonam JadhavMayuri KarandeAbhishek SarkarShubhrakanta SahuDeepaneeta SarmahAishika DattaAntra ChaudharyKiran KaliaArvind SharmaXin WangPallab BhattacharyaPublished in: Cellular and molecular neurobiology (2022)
As the second-leading cause of death, stroke faces several challenges in terms of treatment because of the limited therapeutic interventions available. Previous studies primarily focused on metabolic and blood flow properties as a target for treating stroke, including recombinant tissue plasminogen activator and mechanical thrombectomy, which are the only USFDA approved therapies. These interventions have the limitation of a narrow therapeutic time window, the possibility of hemorrhagic complications, and the expertise required for performing these interventions. Thus, it is important to identify the contributing factors that exacerbate the ischemic outcome and to develop therapies targeting them for regulating cellular homeostasis, mainly neuronal survival and regeneration. Glial cells, primarily microglia, astrocytes, and oligodendrocytes, have been shown to have a crucial role in the prognosis of ischemic brain injury, contributing to inflammatory responses. They play a dual role in both the onset as well as resolution of the inflammatory responses. Understanding the different mechanisms driving these effects can aid in the development of therapeutic targets and further mitigate the damage caused. In this review, we summarize the functions of various glial cells and their contribution to stroke pathology. The review highlights the therapeutic options currently being explored and developed that primarily target glial cells and can be used as neuroprotective agents for the treatment of ischemic stroke.
Keyphrases
- induced apoptosis
- brain injury
- atrial fibrillation
- cerebral ischemia
- cell cycle arrest
- blood flow
- neuropathic pain
- subarachnoid hemorrhage
- stem cells
- endoplasmic reticulum stress
- oxidative stress
- cell death
- risk factors
- signaling pathway
- inflammatory response
- ischemia reperfusion injury
- drug delivery
- cancer therapy
- cell free
- smoking cessation