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Another possible reason is that tumour hypoxemia resulting from anti–VEGF-A/VEGFR therapy lead to the over-expression of matrix components that bind and sequester VEGF-A, rendering anti-VEGF drugs ineffective [86]
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10,11,12 UA, mediates the innate immune response, which can release inflammatory mediators and activate the renin-angiotensin system, 13 inflammatory responses, oxidative stress, vascular endothelial dysfunction and insulin resistance
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