ArticleJournal of the American Society of Nephrology : JASN2016
ADAMTS13 Endopeptidase Protects against Vascular Endothelial Growth Factor Inhibitor-Induced Thrombotic Microangiopathy.
Article in Journal of the American Society of Nephrology : JASN, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 16 citations in OpenAlex.
- Biopsy-proven tyrosine kinase inhibitor-associated renal injury: a case series.Clinical kidney journal · 2026Article
- Development of a protease-resistant ADAMTS13 to improve stability against proteolytic degradation.Blood advances · 2025Article
- A half-century of VEGFA: from theory to practice.The Journal of clinical investigation · 2024Article
- Mechanisms of ADAMTS13 regulation.Journal of thrombosis and haemostasis : JTH · 2022Review
- Impaired renal reserve contributes to preeclampsia via the kynurenine and soluble fms-like tyrosine kinase 1 pathway.The Journal of clinical investigation · 2022Article
- ADAMTS13: An Emerging Target in Stroke Therapy.Frontiers in neurology · 2019Review
- Hepatic dysfunction and thrombocytopenia induced by excess sFlt1 in mice lacking endothelial nitric oxide synthase.Scientific reports · 2018Article
- ADAMTS13 Retards Progression of Diabetic Nephropathy by Inhibiting Intrarenal Thrombosis in Mice.Arteriosclerosis, thrombosis, and vascular biology · 2017Article
- PAD4 Deficiency Decreases Inflammation and Susceptibility to Pregnancy Loss in a Mouse Model.Biology of reproduction · 2016Article
- Plasma von Willebrand factor levels predict in-hospital survival in patients with acute-on-chronic liver failure.Indian journal of gastroenterology : official journal of the Indian Society of Gastroenterology · 2016Article
- Endothelial Dysfunction: The Secret Agent Driving Kidney Disease.Journal of the American Society of Nephrology : JASN · 2016Article
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8 authors at 3 institutions in 1 country.
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Abstract
Thrombotic microangiopathy (TMA) is a life-threatening condition that affects some, but not all, recipients of vascular endothelial growth factor (VEGF) inhibitors given as part of chemotherapy. TMA is also a complication of preeclampsia, a disease characterized by excess production of the VEGF-scavenging soluble VEGF receptor 1 (soluble fms-like tyrosine kinase 1; sFlt-1). Risk factors for VEGF inhibitor-related TMA remain unknown. We hypothesized that deficiency of the VWF-cleaving ADAMTS13 endopeptidase contributes to the development of VEGF inhibitor-related TMA. ADAMTS13(-/-) mice overexpressing sFlt-1 presented all hallmarks of TMA, including thrombocytopenia, schistocytosis, anemia, and VWF-positive microthrombi in multiple organs. Similar to VEGF inhibitor-related TMA in humans, these mice exhibited severely impaired kidney function and hypertension. In contrast, wild-type mice overexpressing sFlt-1 developed modest hypertension but no other features of TMA. Recombinant ADAMTS13 therapy ameliorated all symptoms of TMA in ADAMTS13(-/-) mice overexpressing sFlt-1 and normalized BP in wild-type mice. ADAMTS13 activity may thus be a critical determinant for the development of TMA secondary to VEGF inhibition. Administration of recombinant ADAMTS13 may serve as a therapeutic approach to treat or prevent thrombotic complications of VEGF inhibition.
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