Journal
NEUROLOGICAL SCIENCES
Volume 38, Issue 7, Pages 1167-1186Publisher
SPRINGER-VERLAG ITALIA SRL
DOI: 10.1007/s10072-017-2938-1
Keywords
Ischemia; Stroke; Oxidative stress; Inflammation; Apoptosis
Categories
Funding
- Ahvaz Jundishapur University Grant
Ask authors/readers for more resources
Stroke is the second most common cause of death and the leading cause of disability worldwide. Brain injury following stroke results from a complex series of pathophysiological events including excitotoxicity, oxidative and nitrative stress, inflammation, and apoptosis. Moreover, there is a mechanistic link between brain ischemia, innate and adaptive immune cells, intracranial atherosclerosis, and also the gut microbiota in modifying the cerebral responses to ischemic insult. There are very few treatments for stroke injuries, partly owing to an incomplete understanding of the diverse cellular and molecular changes that occur following ischemic stroke and that are responsible for neuronal death. Experimental discoveries have begun to define the cellular and molecular mechanisms involved in stroke injury, leading to the development of numerous agents that target various injury pathways. In the present article, we review the underlying pathophysiology of ischemic stroke and reveal the intertwined pathways that are promising therapeutic targets.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available