of vascular endothelial growth factor (VEGF). As
normal retinal vascularization occurs, VEGF is
present, causing a "wave of 'physiological hypoxia'" (Chen & Smith, 2007) guiding vessel
growth outward from the optic nerve. VEGF follows this wave and stimulates vessel
growth. When infants receive more oxygen than
they would in utero, due to premature birth and
exposure to room air or oxygen therapy, this
wave is interrupted, halting vessel growth. In response to the ceased vessel growth and hypoxic
environment created by this halt, VEGF increases
and neovascularization occurs, causing abnormal
vessels and scarring. It is theorized that correctly
timed administering of anti-VEGF and VEGF can
mimic the natural occurrence of this process in
the development of the eye and prevent ROP by
preventing the loss of blood vessels, therefore
preventing the response - proliferation of abnormal vessels (Chen & Smith, 2007). The use of
bevacizumab, an anti-VEGF molecule, has only
been used in animal models thus far. The timing
of the use of anti-VEGF and VEGF is absolutely
critical, contrary to each other, and has not been
perfected (Agarwal, Azad, Chandra, Chawla,
Deorari, & Paul, 2012). This research seems
quite promising to me, as it attempts to mimic the
natural development of the eye vessels, preventing ROP rather than ameliorating the problem after it occurs. Also noted in the Chen article is that
insulin-like growth factor (GH/IGF-1) triggers the
production of VEGF and increases as the gestational age of the newborn increases. IGF-1 is
also correlated to brain development and lower
levels of this hormone may not only cause lower
levels of VEGF and interrupt eye development,
but may also contribute to "abnormal neural retinal function" due to delayed brain development,
further jeopardizing visual function (Chen &
Smith, 2007).
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