Increased neovascularization in mice lacking tissue inhibitor of metalloproteinases-3. - Wikidata - wikimedia - TriplyDB

Increased neovascularization in mice lacking tissue inhibitor of metalloproteinases-3.

Increased neovascularization in mice lacking tissue inhibitor of metalloproteinases-3.

http://www.wikidata.org/entity/Q33808182

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Can Novel Treatment of Age-Related Macular Degeneration Be Developed by Better Understanding of Sorsby's Fundus Dystrophy Tissue inhibitor of metalloproteinases-3 peptides inhibit angiogenesis and choroidal neovascularization in mice Intravitreal injection of TIMP3 or the EGFR inhibitor erlotinib offers protection from oxygen-induced retinopathy in mice.Serum levels of matrix metalloproteinase 2 and matrix metalloproteinase 9 elevated in polypoidal choroidal vasculopathy but not in age-related macular degeneration Abnormal recruitment of extracellular matrix proteins by excess Notch3 ECD: a new pathomechanism in CADASIL A peptide derived from TIMP-3 inhibits multiple angiogenic growth factor receptors and tumour growth and inflammatory arthritis in mice.Recent drug therapies for corneal neovascularization.Tissue inhibitor of metalloproteinases 3-dependent microvascular endothelial cell barrier function is disrupted under septic conditions.Calcifying Cystic Odontogenic Tumour: immunohistochemical expression of matrix metalloproteinases, their inhibitors (TIMPs and RECK) and inducer (EMMPRIN).STAT3-mediated activation of miR-21 is involved in down-regulation of TIMP3 and neovascularization in the ischemic retina.

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Increased neovascularization in mice lacking tissue inhibitor of metalloproteinases-3.

http://www.wikidata.org/entity/Q33808182

description

2011 nî lūn-bûn

@nan

2011 թուականի Օգոստոսին հրատարակուած գիտական յօդուած

@hyw

2011 թվականի օգոստոսին հրատարակված գիտական հոդված

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2011年の論文

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2011年論文

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2011年論文

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2011年論文

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2011年論文

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2011年論文

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2011年论文

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name

Increased neovascularization in mice lacking tissue inhibitor of metalloproteinases-3.

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Increased neovascularization in mice lacking tissue inhibitor of metalloproteinases-3.

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type

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Increased neovascularization in mice lacking tissue inhibitor of metalloproteinases-3.

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Increased neovascularization in mice lacking tissue inhibitor of metalloproteinases-3.

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Increased neovascularization in mice lacking tissue inhibitor of metalloproteinases-3.

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Investigative Ophthalmology & Visual Science

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Increased neovascularization in mice lacking tissue inhibitor of metalloproteinases-3.

@en

P2093

Alecia Cutler

http://www.w3.org/2001/XMLSchema#string

Amit Vasanji

http://www.w3.org/2001/XMLSchema#string

Bela Anand-Apte

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Jian Hua Qi

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Jonathan E Sears

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Mariya Ali

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Masahiko Sugimoto

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Quteba Ebrahem

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Rama Khokha

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P2860

CFH, C3 and ARMS2 are significant risk loci for susceptibility but not for disease progression of geographic atrophy due to AMD

A common haplotype in the complement regulatory gene factor H (HF1/CFH) predisposes individuals to age-related macular degeneration

Complement factor H polymorphism in age-related macular degeneration

Genetic variants near TIMP3 and high-density lipoprotein-associated loci influence susceptibility to age-related macular degeneration

A novel function for tissue inhibitor of metalloproteinases-3 (TIMP3): inhibition of angiogenesis by blockage of VEGF binding to VEGF receptor-2

Mutations in the tissue inhibitor of metalloproteinases-3 (TIMP3) in patients with Sorsby's fundus dystrophy

Complement factor H variant increases the risk of age-related macular degeneration

The gene structure of tissue inhibitor of metalloproteinases (TIMP)-3 and its inhibitory activities define the distinct TIMP gene family

Intrachoroidal neovascularization in transgenic mice overexpressing vascular endothelial growth factor in the retinal pigment epithelium

Vascular endothelial growth factor expression in the retinal pigment epithelium is essential for choriocapillaris development and visual function

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6117-6123

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10.1167/IOVS.10-5899

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9

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neovascularization

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