AMD: Gene Expression Pathways React Differently to Various Anti-VEGF Drugs
AUGUST 10, 2016
Baruch Kuppermann, MD, PhD, a professor of ophthalmology and biomedical engineering at the University of California, Irvine, and colleagues looked at gene expression modifications in retinal Müller cells treated with anti-VEGFs. Speaking at the 34th Annual Scientific Meeting of the American Society of Retina Specialists (ASRS 2016) in San Francisco, California, Kuppermann presented the question – why is there increased atrophy with chronic use of anti-VEGF drugs?
The analysis analyzed four pathways: angiogenesis, antioxidant, inflammation, and apoptosis. The team hypothesized that anti-VEGF drugs can affect non-angiogenesis pathways related to oxidative stress and apoptosis.
The anti-VEGF drugs did indeed induce changes in the gene expressions involved in the pathways. As expected, gene expression decreased with all four drugs through the angiogenesis pathway (VEGFA). Kuppermann noted that “interestingly” there was less of a decrease with ziv-aflibercept.
Dubbed by Kuppermann as the most important finding of the study, the analysis revealed that the gene expression levels of antioxidant enzyme (SOD2) decreased with all four anti-VEGF drugs.
Inflammation (IL-18) showed an increase of gene expression. Apoptosis (BCL2L13) had no change with ranibizumab or ziv-aflibercept, but had an increase with bevacizumab.
“The data supports our hypothesis that exposure to anti-VEGF drugs can cause changes in non-angiogenic pathways,” Kupperman said at ASRS 2016. He concluded the presentation by saying that having a better understanding of the impact of these drugs on retinal cells can help progress in treatment options.
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