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• W2018347789 abstract "Alternative splicing of the gene encoding VEGF-A under ischemic conditions generates an antiangiogenic isoform of the protein that impairs revascularization under conditions of metabolic dysfunction in mice, and this isoform is found at elevated levels in patients with peripheral artery disease. Peripheral artery disease (PAD) generates tissue ischemia through arterial occlusions and insufficient collateral vessel formation. Vascular insufficiency in PAD occurs despite higher circulating levels of vascular endothelial growth factor A (VEGF-A)1,2, a key regulator of angiogenesis. Here we show that clinical PAD is associated with elevated levels of an antiangiogenic VEGF-A splice isoform (VEGF-A165b) and a corresponding reduction in levels of the proangiogenic VEGF-A165a splice isoform. In mice, VEGF-A165b expression was upregulated by conditions associated with impaired limb revascularization, including leptin deficiency, diet-induced obesity, genetic ablation of the secreted frizzled-related protein 5 (Sfrp5) adipokine and transgenic overexpression of Wnt5a in myeloid cells. In a mouse model of PAD, delivery of VEGF-A165b inhibited revascularization of ischemic hind limbs, whereas treatment with an isoform-specific neutralizing antibody reversed impaired revascularization caused by metabolic dysfunction or perturbations in the Wnt5a-Sfrp5 regulatory system. These results indicate that inflammation-driven expression of the antiangiogenic VEGF-A isoform can contribute to impaired collateralization in ischemic cardiovascular disease." @default.
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• W2018347789 date "2014-11-02" @default.
• W2018347789 modified "2023-10-16" @default.
• W2018347789 title "An antiangiogenic isoform of VEGF-A contributes to impaired vascularization in peripheral artery disease" @default.
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• W2018347789 doi "https://doi.org/10.1038/nm.3703" @default.
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