ArticleMolecular and cellular biology2009
ADAM9 is involved in pathological retinal neovascularization.
Article in Molecular and cellular biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
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Who cites it
57 citing papers in PubMed, 94 citations in OpenAlex.
- Adipocytes influence choroidal neovascularization via PRDM16.EMBO molecular medicine · 2026Article
- ADAM9: an updated view of its biology and pathology.Molecular biology reports · 2026Review
- ADAM9 in tumor biology: molecular functions, clinical implications, and therapeutic targeting.Cellular & molecular biology letters · 2026Review
- The ADAM Family of Proteases: Structure, Substrates, and Roles in Liver Diseases.International journal of molecular sciences · 2026Review
- Chromosome-level genome assembly and single-cell analysis unveil molecular mechanisms of arm regeneration in the ophiuroid Ophiura sarsii vadicola.Genome biology · 2025Article
- Perturbation of EPHA2 and EFNA1iScience · 2025Article
- Hypoxia Promotes the Expression of ADAM9 by Tubular Epithelial Cells, Which Enhances Transforming Growth Factor β1 Activation and Promotes Tissue Fibrosis in Patients With Lupus Nephritis.Arthritis & rheumatology (Hoboken, N.J.) · 2025Article
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- Identifications of novel host cell factors that interact with the receptor-binding domain of the SARS-CoV-2 spike protein.The Journal of biological chemistry · 2024Article
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- Non-coding RNAs and glioblastoma: Insight into their roles in metastasis.Molecular therapy oncolytics · 2022Review
- Inhibition of Vascular Growth by Modulation of the Anandamide/Fatty Acid Amide Hydrolase Axis.Arteriosclerosis, thrombosis, and vascular biology · 2021Article
- ADAM9 enhances Th17 cell differentiation and autoimmunity by activating TGF-β1.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Contribution of ADAM17 and related ADAMs in cardiovascular diseases.Cellular and molecular life sciences : CMLS · 2021Review
- Analysis of ADAM9 regulation and function in vestibular schwannoma primary cells.BMC research notes · 2020Article
- Review
- An Overview of ADAM9: Structure, Activation, and Regulation in Human Diseases.International journal of molecular sciences · 2020Review
- MicroRNA-126-3p Inhibits Angiogenic Function of Human Lung Microvascular Endothelial Cells via LAT1 (L-Type Amino Acid Transporter 1)-Mediated mTOR (Mammalian Target of Rapamycin) Signaling.Arteriosclerosis, thrombosis, and vascular biology · 2020Article
- Transcriptome analyses reveal molecular mechanisms underlying phenotypic differences among transcriptional subtypes of glioblastoma.Journal of cellular and molecular medicine · 2020Article
- Proteome and Secretome Dynamics of Human Retinal Pigment Epithelium in Response to Reactive Oxygen Species.Scientific reports · 2019Article
Corrections and comments
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Authors and funding
6 authors at 5 institutions in 1 country.
Funding
Abstract
Pathological ocular neovascularization, caused by diabetic retinopathy, age-related macular degeneration, or retinopathy of prematurity, is a leading cause of blindness, yet much remains to be learned about its underlying causes. Here we used oxygen-induced retinopathy (OIR) and laser-induced choroidal neovascularization (CNV) to assess the contribution of the metalloprotease-disintegrin ADAM9 to ocular neovascularization in mice. Pathological neovascularization in both the OIR and CNV models was significantly reduced in Adam9(-/-) mice compared to wild-type controls. In addition, the level of ADAM9 expression was strongly increased in endothelial cells in pathological vascular tufts in the OIR model. Moreover, tumor growth from heterotopically injected B16F0 melanoma cells was reduced in Adam9(-/-) mice compared to controls. In cell-based assays, the overexpression of ADAM9 enhanced the ectodomain shedding of EphB4, Tie-2, Flk-1, CD40, VCAM, and VE-cadherin, so the enhanced expression of ADAM9 could potentially affect pathological neovascularization by increasing the shedding of these and other membrane proteins from endothelial cells. Finally, we provide the first evidence for the upregulation of ADAM9-dependent shedding by reactive oxygen species, which in turn are known to play a critical role in OIR. Collectively, these results suggest that ADAM9 could be an attractive target for the prevention of proliferative retinopathies, CNV, and cancer.
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Registered trials
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