Abstract
In recent years, growth factor therapy has emerged as a potential treatment for ischemic brain injury. The efficacy of therapies that either directly introduce or stimulate local production of growth factors and their receptors in damaged brain tissue has been tested in a multitude of models for different Central Nervous System (CNS) diseases. These growth factors include erythropoietin (EPO), vascular endothelial growth factor (VEGF), brain-derived neurotrophic factor (BDNF), and insulin-like growth factor (IGF-1), among others. Despite the promise shown in animal models, the particular growth factors that should be used to maximize both brain protection and repair, and the therapeutic critical period, are not well defined. We will review current pre-clinical and clinical evidence for growth factor therapies in treating different causes of brain injury, as well as issues to be addressed prior to application in humans.
Highlights
Hypoxic-ischemic injury is a significant cause of mortality and morbidity in both the adult and immature subject
vascular endothelial growth factor (VEGF)-A is the key mediator of arteriogenesis in the brain and is upregulated following stroke in rats, leading to increased post-ischemic angiogenesis and decreased infarct volume [30]
Lower brain-derived neurotrophic factor (BDNF) and higher VEGF levels were associated with increased risk of having a transient ischemic attack
Summary
Hypoxic-ischemic injury is a significant cause of mortality and morbidity in both the adult and immature subject. Endogenous response mechanisms following exposure to hypoxia-ischemia includes the stabilization of neuronal transcription factors hypoxia-inducible factors (HIF)-1 and 2, with increased expression of a number of downstream cytokines and growth factors. These growth factors play important roles in normal central nervous system development and function, and this increased expression following injury activates a number of signaling pathways that mediate changes in apoptosis, inflammation, angiogenesis, cell differentiation and proliferation. Despite these endogenous repair processes, significant deficits persist. Additional therapies that both lengthen the therapeutic window for treatment and enhance this long-term repair are critical for improving outcomes
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