18.188.162.87=18.1
https://eutils.ncbi.nlm.nih.gov/entrez/eutils/efetch.fcgi?db=pubmed&id=24875332&retmode=xml&tool=pubfacts&email=info@pubfacts.com&api_key=b8daa3ad693db53b1410957c26c9a51b490818.188.162.87=18.1
https://eutils.ncbi.nlm.nih.gov/entrez/eutils/esearch.fcgi?db=pubmed&term=cerebral+ischemia&datetype=edat&usehistory=y&retmax=5&tool=pubfacts&email=info@pubfacts.com&api_key=b8daa3ad693db53b1410957c26c9a51b4908 Axon guidance factor netrin-1 and its receptors regulate angiogenesis after cerebral ischemia. | LitMetric

Axon guidance factor netrin-1 and its receptors regulate angiogenesis after cerebral ischemia.

Neurosci Bull

Department of Neurology, Guangdong Key Laboratory for Diagnosis and Treatment of Major Neurological Diseases, National Key Clinical Department, National Key Discipline, the First Affiliated Hospital of Sun Yat-Sen University, Guangzhou, 510080, China.

Published: August 2014

Neurogenesis and angiogenesis play important roles in functional recovery after ischemic stroke. When cerebral ischemia occurs, axon regeneration can compensate for the loss of apoptotic neurons in the ischemic area. The formation of new blood vessels ameliorates the local decrease in blood supply, enhancing the supply of oxygen and nutrients to newly-formed neurons. New blood vessels also act as a scaffold for the migration of neuroblasts to the infarct area after ischemic stroke. In light of this, researchers have been actively searching for methods to treat cerebral infarction. Netrins were first identified as a family of proteins that mediate axon guidance and direct axon migration during embryogenesis. Later studies have revealed other functions of this protein family. In this review, we focus on netrin-1, which has been shown to be involved in axon migration and angiogenesis, which are required for recovery after cerebral ischemia. Thus, therapies targeting netrin-1 may be useful for the treatment of ischemic stroke.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5562620PMC
http://dx.doi.org/10.1007/s12264-013-1441-9DOI Listing

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