BEYOND REAOSN
sulfur amino acid(단백질 제한식이)는 VEGF자극을 통해 암세포의 혈관신생을 자극함
그리고 Hypoxia is the best-understood trigger of VEGF expression via the transcription factor HIF1a.
SUMMARY
Angiogenesis, the formation of new blood vessels by endothelial cells (ECs), is an adaptive response to oxygen/nutrient deprivation orchestrated by vascular endothelial growth factor (VEGF) upon ischemia or exercise. Hypoxia is the best-understood trigger of VEGF expression via the transcription factor HIF1a. Nutrient deprivation is inseparable from hypoxia during ischemia, yet its role in angiogenesis is poorly characterized.
Here, we identified sulfur amino acid restriction as a proangiogenic trigger, promoting increased VEGF expression, migration and sprouting in ECs in vitro, and increased capillary density in mouse skeletal muscle in vivo via the GCN2/ATF4 amino acid starvation response pathway independent of hypoxia or HIF1a.
We also identified a
requirement for cystathionine-g-lyase in VEGF-
dependent angiogenesis via increased hydrogen
sulfide (H2S) production. H2S mediated its proangiogenic effects in part by inhibiting mitochondrial
electron transport and oxidative phosphorylation, resulting in increased glucose uptake and glycolytic
ATP production.