ArticleProceedings of the National Academy of Sciences of the United States of America2013
Anti-VEGF- and anti-VEGF receptor-induced vascular alteration in mouse healthy tissues.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 102 papers.
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Who cites it
102 citing papers in PubMed, 137 citations in OpenAlex.
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- Strategic drug sequencing in hepatocellular carcinoma in the era of chemo-diversity: maximizing the therapeutic benefit of lenvatinib.Journal of liver cancer · 2026Review
- Coviretinopathy: COVID-19-induced VEGF-dependent retinopathy.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- PIEZO1 Mediates Apoptosis of Endothelial Cells via Enhancing HMGA2 Expression Under Simulated Microgravity.International journal of molecular sciences · 2026Article
- Impact of Antivascular Endothelial Growth Factor Therapy in Chronic Subdural Hematoma Patients: A Propensity-Matched Multi-Institutional Cohort Study.Stroke (Hoboken, N.J.) · 2026Article
- Multiscale profiling of tyrosine kinase inhibitor cardiotoxicity reveals mechanosensitive ion channel PIEZO1 as cardioprotective.Science translational medicine · 2025Article
- Research Progress Regarding the Use of Single-Cell Sequencing Technology in Analyzing Tumor Endothelial Cell Pathophysiology.International journal of molecular sciences · 2025Review
- Effects of cabozantinib on plasma adrenocorticotropic hormone and serum cortisol levels in patients with metastatic renal cell carcinoma: a retrospective study.BMC endocrine disorders · 2025Article
- Fatal portal vein thrombosis following combination therapy with atezolizumab plus bevacizumab for hepatocellular carcinoma: an autopsy case report.Clinical journal of gastroenterology · 2025Article
- Angiopoietin-TIE2 feedforward circuit promotes PIK3CA-driven venous malformations.Nature cardiovascular research · 2025Article
- Obesity drives depot-specific vascular remodeling in male white adipose tissue.Nature communications · 2025Article
- Vascular endothelial growth factor signaling in health and disease: from molecular mechanisms to therapeutic perspectives.Signal transduction and targeted therapy · 2025Review
- Effects of Lenvatinib treatment for advanced differentiated thyroid cancer on cortisol deficiency.Frontiers in endocrinology · 2025Article
- Review
- Suppression of matrigel-induced choroidal neovascularization by AAV delivery of a novel anti-Scg3 antibody.Gene therapy · 2024Article
- Celebrating the 1945 JNCI pioneering contribution to antiangiogenic therapy for cancer.Journal of the National Cancer Institute · 2024Article
- Effective Prevention and Treatment of Acute Leukemias in Mice by Activation of Thermogenic Adipose Tissues.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Towards Targeting Endothelial Rap1B to Overcome Vascular Immunosuppression in Cancer.International journal of molecular sciences · 2024Review
- Nanotherapy to Reshape the Tumor Microenvironment: A New Strategy for Prostate Cancer Treatment.ACS omega · 2024Review
42 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Systemic therapy with anti-VEGF drugs such as bevacizumab is widely used for treatment of human patients with various solid tumors. However, systemic impacts of such drugs in host healthy vasculatures remain poorly understood. Here, we show that, in mice, systemic delivery of an anti-VEGF or an anti-VEGF receptor (VEGFR)-2 neutralizing antibody caused global vascular regression. Among all examined tissues, vasculatures in endocrine glands, intestinal villi, and uterus are the most affected in response to VEGF or VEGFR-2 blockades. Thyroid vascular fenestrations were virtually completely blocked by VEGF blockade, leading to marked accumulation of intraendothelial caveolae vesicles. VEGF blockade markedly increased thyroid endothelial cell apoptosis, and withdrawal of anti-VEGF resulted in full recovery of vascular density and architecture after 14 d. Prolonged anti-VEGF treatment resulted in a significant decrease of the circulating level of the predominant thyroid hormone free thyroxine, but not the minimal isoform of triiodothyronine, suggesting that chronic anti-VEGF treatment impairs thyroid functions. Conversely, VEGFR-1-specific blockade produced virtually no obvious phenotypes. These findings provide structural and functional bases of anti-VEGF-specific drug-induced side effects in relation to vascular changes in healthy tissues. Understanding anti-VEGF drug-induced vascular alterations in healthy tissues is crucial to minimize and even to avoid adverse effects produced by currently used anti-VEGF-specific drugs.
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Registered trials
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.