ArticleScience translational medicine2010
A monoclonal antibody against alphaVbeta3 integrin inhibits development of atherosclerotic lesions in diabetic pigs.
Article in Science translational medicine, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 41 citations in OpenAlex.
- Evaluation of an Integrin αNuclear medicine and molecular imaging · 2023Article
- Crosstalk Between Macrophages and Vascular Smooth Muscle Cells in Atherosclerotic Plaque Stability.Arteriosclerosis, thrombosis, and vascular biology · 2022Review
- Membrane cholesterol and substrate stiffness co-ordinate to induce the remodelling of the cytoskeleton and the alteration in the biomechanics of vascular smooth muscle cells.Cardiovascular research · 2019Article
- IGF-1 and cardiovascular disease.Growth hormone & IGF research : official journal of the Growth Hormone Research Society and the International IGF Research Society · 2019Review
- Applying nanomedicine in maladaptive inflammation and angiogenesis.Advanced drug delivery reviews · 2017Review
- Integrin signaling in atherosclerosis.Cellular and molecular life sciences : CMLS · 2017Review
- Article
- Developing Treatments for Chronic Kidney Disease in the 21st Century.Seminars in nephrology · 2016Review
- The next generation of therapeutics for chronic kidney disease.Nature reviews. Drug discovery · 2016Review
- Positron emission tomography imaging of coronary atherosclerosis.Future cardiology · 2016Review
- Rational design of a protein that binds integrin αvβ3 outside the ligand binding site.Nature communications · 2016Article
- The arterial microenvironment: the where and why of atherosclerosis.The Biochemical journal · 2016Review
- Integrin β3 inhibition is a therapeutic strategy for supravalvular aortic stenosis.The Journal of experimental medicine · 2016Article
- Hyperglycemia stimulates p62/PKCζ interaction, which mediates NF-κB activation, increased Nox4 expression, and inflammatory cytokine activation in vascular smooth muscle.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2015Article
- αvβ3 Integrins Mediate Flow-Induced NF-κB Activation, Proinflammatory Gene Expression, and Early Atherogenic Inflammation.The American journal of pathology · 2015Article
- Blocking ligand occupancy of the αVβ3 integrin inhibits the development of nephropathy in diabetic pigs.Endocrinology · 2014Article
- Structural basis for pure antagonism of integrin αVβ3 by a high-affinity form of fibronectin.Nature structural & molecular biology · 2014Article
- Blocking αVβ3 integrin ligand occupancy inhibits the progression of albuminuria in diabetic rats.Journal of diabetes research · 2014Article
- Article
- Importance of receptor-targeted systems in the battle against atherosclerosis.Current pharmaceutical design · 2013Review
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Atherosclerotic lesions develop and progress more rapidly in diabetic patients than in nondiabetic individuals. This may be caused by accelerated lesion formation in the high-glucose environment of diabetes. Smooth muscle cells (SMCs) cultured in high glucose are more responsive to growth factors such as insulin-like growth factor-1 (IGF-1). This enhanced response to IGF-1 is due in part to increased activation of the alpha(V)beta(3) integrin. We tested whether alpha(V)beta(3) integrin activation was increased in diabetic animals and whether an antibody to beta(3) would inhibit IGF-1 action and development of atherosclerosis. Eight male pigs were made diabetic with streptozotocin and fed a high-fat diet. A F(ab)(2) antibody fragment directed at beta(3) was infused into one femoral artery, whereas the other artery received control F(ab)(2) for 3.5 months. There was a 65 +/- 8% reduction in atherosclerotic lesion area in the arteries treated with F(ab)(2) antibody to beta(3). Phosphorylation of beta(3) was reduced by 75 +/- 18% in vessels treated with the antibody. Shc and mitogen-activated protein kinase phosphorylation, which are required for IGF-1-stimulated SMC proliferation, were also significantly reduced. We conclude that activation of IGF-1 receptor and alpha(V)beta(3)-linked signaling pathways accelerates atherosclerosis in diabetes and that administration of an antibody to beta(3) to diabetic pigs inhibits alpha(V)beta(3) activation, IGF-1-stimulated signaling, and atherosclerotic lesion development. This approach offers a potential therapeutic approach to the treatment of this 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 OpenQuestion graph.