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Von Hippel‐Lindau tumor suppressor and HIF‐1α: new targets of NSAID inhibition of hypoxia‐induced angiogenesis
NSAIDs may block low-oxygen blood vessel growth by targeting VHL tumor suppressor and HIF-1alpha
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Abstract
Both nonselective and COX-2-selective NSAIDs inhibit hypoxia-induced angiogenesis in gastric microvascular endothelial cells.
- NSAIDs increase the expression of the von Hippel-Lindau (VHL) tumor suppressor, which helps target proteins for degradation.
- This increase in VHL leads to reduced levels of hypoxia-inducible factor-1alpha (HIF-1alpha), a key regulator of blood vessel growth.
- Lower HIF-1alpha levels result in decreased expression of vascular endothelial growth factor (VEGF) and its receptor Flt-1, which are critical for angiogenesis.
- NSAIDs' inhibition of angiogenesis may have both prostaglandin-dependent and prostaglandin-independent mechanisms.
- The addition of exogenous VEGF and, to a lesser extent, prostaglandins can partially reverse the inhibitory effects of NSAIDs on angiogenesis.
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