ArticleNature medicine2014
An antiangiogenic isoform of VEGF-A contributes to impaired vascularization in peripheral artery disease.
Article in Nature medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 114 papers.
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Who cites it
114 citing papers in PubMed, 195 citations in OpenAlex.
- Review
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- Profiling of main regulators of angiogenesis and inflammation in human PBMC and plasma revealed associations with lower extremity artery disease.Scientific reports · 2025Article
- Molecular Signatures Related to Inflammation and Angiogenesis in Patients with Lower Extremity Artery Disease, Abdominal Aortic Aneurysm, and Varicose Veins: Shared and Distinct Pathways.International journal of molecular sciences · 2025Article
- Splicing factor kinase SRPK1 inhibition in monocyte: a novel therapeutic approach for peripheral arterial disease.American journal of physiology. Heart and circulatory physiology · 2025Article
- Investigating the Sexual Dimorphism of Waist-to-Hip Ratio and Its Associations with Complex Traits.Genes · 2025Article
- Vascular endothelial growth factor signaling in health and disease: from molecular mechanisms to therapeutic perspectives.Signal transduction and targeted therapy · 2025Review
- Blood biomarkers of vascular dysfunction in small vessel disease progression: Insights from a longitudinal neuroimaging study.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Macrophage Proangiogenic VEGF-A Is Required for Inflammatory Arteriogenesis During Vascular Injury.Biomedicines · 2025Article
- Comprehensive multi-omics analysis elucidates colchicine-induced toxicity mechanisms and unveils the therapeutic potential of MLN4924 and kinase inhibitors.Acta pharmacologica Sinica · 2025Article
- Multi-INTACT: integrative analysis of the genome, transcriptome, and proteome identifies causal mechanisms of complex traits.Genome biology · 2025Article
- Potential antitumoral effects of SRPK1 inhibition through modulation of VEGF splicing in pituitary somatotroph tumoral cells.Frontiers in endocrinology · 2025Article
- Synthetic Antiangiogenic Vascular Endothelial Growth Factor-A Splice Variant Revascularizes Ischemic Muscle in Peripheral Artery Disease.Journal of the American Heart Association · 2024Article
- Tumor Explants Elucidate a Cascade of Paracrine SHH, WNT, and VEGF Signals Driving Pancreatic Cancer Angiosuppression.Cancer discovery · 2024Article
- Large-scale comparison of machine learning methods for profiling prediction of kinase inhibitors.Journal of cheminformatics · 2024Article
- Ischemia-reperfusion injury: molecular mechanisms and therapeutic targets.Signal transduction and targeted therapy · 2024Review
- Inhibiting anti-angiogenic VEGF165b activates a miR-17-20a-Calcipressin-3 pathway that revascularizes ischemic muscle in peripheral artery disease.Communications medicine · 2024Article
- Biology and therapeutic targeting of vascular endothelial growth factor A.Nature reviews. Molecular cell biology · 2023Review
- Article
- Prospects of potential adipokines as therapeutic agents in obesity-linked atherogenic dyslipidemia and insulin resistance.The Egyptian heart journal : (EHJ) : official bulletin of the Egyptian Society of Cardiology · 2023Review
54 more citing papers are in PubMed but not listed here.
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Authors and funding
16 authors at 6 institutions in 3 countries.
Funding
Abstract
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), 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.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.