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Review
. 2016 Jan;11(1):174-9.
doi: 10.4103/1673-5374.175067.

Vascular endothelial growth factor: an attractive target in the treatment of hypoxic/ischemic brain injury

Affiliations
Review

Vascular endothelial growth factor: an attractive target in the treatment of hypoxic/ischemic brain injury

Hui Guo et al. Neural Regen Res. 2016 Jan.

Abstract

Cerebral hypoxia or ischemia results in cell death and cerebral edema, as well as other cellular reactions such as angiogenesis and the reestablishment of functional microvasculature to promote recovery from brain injury. Vascular endothelial growth factor is expressed in the central nervous system after hypoxic/ischemic brain injury, and is involved in the process of brain repair via the regulation of angiogenesis, neurogenesis, neurite outgrowth, and cerebral edema, which all require vascular endothelial growth factor signaling. In this review, we focus on the role of the vascular endothelial growth factor signaling pathway in the response to hypoxic/ischemic brain injury, and discuss potential therapeutic interventions.

Keywords: Akt/eNOS pathway; HIF1; JAK/STAT; PI3K/Akt pathway; Src-SSeCKS pathway; VEGF; VEGFR; hypoxic/ischemic brain injury; nerve regeneration; neural regeneration.

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Conflict of interest statement

Conflicts of interest: None declared.

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References

    1. Akiyama C, Yuguchi T, Nishio M, Tomishima T, Fujinaka T, Taniguchi M, Nakajima Y, Kohmura E, Yoshimine T. Src family kinase inhibitor PP1 reduces secondary damage after spinal cord compression in rats. J Neurotrauma. 2004;21:923–931. - PubMed
    1. Arai K, Jin G, Navaratna D, Lo EH. Brain angiogenesis in developmental and pathological processes: neurovascular injury and angiogenic recovery after stroke. FEBS J. 2009;276:4644–4652. - PMC - PubMed
    1. Baburamani AA, Castillo-Melendez M, Walker DW. VEGF expression and microvascular responses to severe transient hypoxia in the fetal sheep brain. Pediatr Res. 2013;73:310–316. - PubMed
    1. Bai Y, Xu G, Xu M, Li Q, Qin X. Inhibition of Src phosphorylation reduces damage to the blood-brain barrier following transient focal cerebral ischemia in rats. Int J Mol Med. 2014;34:1473–1482. - PMC - PubMed
    1. Bauer AT, Burgers HF, Rabie T, Marti HH. Matrix metalloproteinase-9 mediates hypoxia-induced vascular leakage in the brain via tight junction rearrangement. J Cereb Blood Flow Metab. 2010;30:837–848. - PMC - PubMed