ArticleScience advances2023
A ligand-independent Tie2-activating antibody reduces vascular leakage in models of Clarkson disease.
Article in Science advances, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 9 citations in OpenAlex.
- A novel Tie2xVEGF bispecific antibody fusion demonstrates enhanced therapeutic efficacy through direct Tie2 activation and VEGF neutralization.Journal of translational medicine · 2026Article
- Neutrophil extracellular traps-associated candidate genes in IgA vasculitis: an exploratory multi-omics analysis integrating transcriptomics and Mendelian randomization.Pediatric rheumatology online journal · 2026Article
- Association between the aggregate index of systemic inflammation and 28- or 365-day mortality in acute myocardial infarction patients: insights from the MIMIC-IV database.BMC cardiovascular disorders · 2025Article
- An immune competent in vitro model of IL2 induced vascular leakage enables mechanistic insights and evaluation of mitigation strategies.Scientific reports · 2025Article
- Tie2 activator 4E2 ameliorates diabetic nephropathy and synergizes with dapagliflozin in a mouse model.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2025Article
- Article
- Systemic capillary leak syndrome.Nature reviews. Disease primers · 2024Review
- Article
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Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
Abstract
Vascular dysfunction resulting from endothelial hyperpermeability is a common and important feature of critical illness due to sepsis, trauma, and other conditions associated with acute systemic inflammation. Clarkson disease [monoclonal gammopathy-associated idiopathic systemic capillary leak syndrome (ISCLS)] is a rare, orphan disorder marked by spontaneous and recurrent episodes of hypotensive shock and peripheral edema due to widespread vascular leakage in peripheral tissues. Mortality from acute flares approaches 30% due to lack of effective therapies. We evaluated a monoclonal antibody (4E2) specific for the endothelial receptor tyrosine kinase Tie2 in ISCLS models. 4E2 activated Tie2 in ISCLS patient-derived endothelial cells and reduced baseline and proinflammatory mediator-induced barrier dysfunction. 4E2 also reduced mortality and/or vascular leakage associated with systemic histamine challenge or influenza infection in the SJL/J mouse model of ISCLS. These findings support a critical role for Tie2 dysregulation in ISCLS and highlight a viable therapeutic approach to this catastrophic disorder.
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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 Socratic graph.