ArticleCirculation research2012
Formin mDia1 mediates vascular remodeling via integration of oxidative and signal transduction pathways.
Article in Circulation research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
58 citing papers in PubMed, 90 citations in OpenAlex.
- Glycation and receptors: coming of AGE in the midst of danger.Nature reviews. Endocrinology · 2026Review
- The AGE-RAGE-DIAPH1 Axis in Type 2 Diabetes and Metabolic Dysfunction: From Carbonyl Stress to Diabetic Myocardial and Neuronal Injury.International journal of molecular sciences · 2026Review
- Deconstructing the RAGE signaling maze: the molecular key to opening a new dimension of ovarian anti-aging.Experimental & molecular medicine · 2026Review
- RAGE-mediated activation of the formin DIAPH1 and human macrophage inflammation are inhibited by a small molecule antagonist.Cell chemical biology · 2025Article
- Mechanistic underpinnings of AGEs-RAGE via DIAPH1 in ischemic, diabetic, and failing hearts.American journal of physiology. Heart and circulatory physiology · 2025Article
- Assessment of cardiac and skeletal muscle metabolites usingNMR in biomedicine · 2025Article
- RAGE/DIAPH1 Axis and Cardiometabolic Disease: From Nascent Discoveries to Therapeutic Potential.Arteriosclerosis, thrombosis, and vascular biology · 2024Review
- RAGE/DIAPH1 and atherosclerosis through an evolving lens: Viewing the cell from the "Inside - Out".Atherosclerosis · 2024Review
- The RAGE Axis: A Relevant Inflammatory Hub in Human Diseases.Biomolecules · 2024Review
- Association between DIAPH1 variant and posterior circulation involvement with Moyamoya disease.Scientific reports · 2023Article
- DIAPH1 mediates progression of atherosclerosis and regulates hepatic lipid metabolism in mice.Communications biology · 2023Article
- Receptor of advanced glycation end-products axis and gallbladder cancer: A forgotten connection that we should reconsider.World journal of gastroenterology · 2022Review
- A Review on Preclinical Models of Ischemic Stroke: Insights Into the Pathomechanisms and New Treatment Strategies.Current neuropharmacology · 2022Review
- The RAGE/DIAPH1 Signaling Axis & Implications for the Pathogenesis of Diabetic Complications.International journal of molecular sciences · 2022Review
- Pathophysiology of RAGE in inflammatory diseases.Frontiers in immunology · 2022Review
- Small-molecule antagonism of the interaction of the RAGE cytoplasmic domain with DIAPH1 reduces diabetic complications in mice.Science translational medicine · 2021Article
- DIAPH1 Variants in Non-East Asian Patients With Sporadic Moyamoya Disease.JAMA neurology · 2021Article
- Molecular Characteristics of RAGE and Advances in Small-Molecule Inhibitors.International journal of molecular sciences · 2021Review
- Glycation reaction and the role of the receptor for advanced glycation end-products in immunity and social behavior.Glycoconjugate journal · 2021Review
- Journey to a Receptor for Advanced Glycation End Products Connection in Severe Acute Respiratory Syndrome Coronavirus 2 Infection: With Stops Along the Way in the Lung, Heart, Blood Vessels, and Adipose Tissue.Arteriosclerosis, thrombosis, and vascular biology · 2021Review
Corrections and comments
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
rationaleThe mammalian diaphanous-related formin (mDia1), governs microtubule and microfilament dynamics while functioning as an effector for Rho small GTP-binding proteins during key cellular processes such as adhesion, cytokinesis, cell polarity, and morphogenesis. The cytoplasmic domain of the receptor for advanced glycation endproducts binds to the formin homology 1 domain of mDia1; mDia1 is required for receptor for advanced glycation endproducts ligand-induced cellular migration in transformed cells.
objectiveBecause a key mechanism in vascular remodeling is the induction of smooth muscle cell migration, we tested the role of mDia1 in this process. METHODS AND
resultsWe report that endothelial denudation injury to the murine femoral artery significantly upregulates mDia1 mRNA transcripts and protein in the injured vessel, particularly in vascular smooth muscle cells within the expanding neointima. Loss of mDia1 expression significantly reduces pathological neointimal expansion consequent to injury. In primary murine aortic smooth muscle cells, mDia1 is required for receptor for advanced glycation endproducts ligand-induced membrane translocation of c-Src, which leads to Rac1 activation, redox phosphorylation of AKT/glycogen synthase kinase 3β, and consequent smooth muscle cell migration.
conclusionsWe conclude that mDia1 integrates oxidative and signal transduction pathways triggered, at least in part, by receptor for advanced glycation endproducts ligands, thereby regulating pathological neointimal expansion.
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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.