Abstract
Ischemic stroke is one of the leading causes of disability and death among adults worldwide. It occurs when blood flow to the brain is interrupted. Currently available treatments for patients with ischemic stroke focus solely on restoring blood flow. Therefore, there is a lack of methods that would accelerate brain regeneration after a stroke or even provide a protective effect. This study describes the role of the astrocyte-secreted protein CHI3L1 (chitinase-3-like protein 1) in the pathophysiology of stroke, as well as other diseases of the central nervous system. The structure of the protein, the receptors to which CHI3L1 binds and the activated signaling pathways along with the resulting biological effects relevant to ischemic stroke are discussed. It is indicated that changes in CHI3L1 levels potentially influence post-stroke regeneration in both humans and animal models. The common mechanisms of CHI3L1 action across various neurological diseases suggest its significant role in the future diagnosis and treatment of ischemic stroke, Alzheimer’s and Parkinson’s diseases, and glioma.