ArticleDisease markers2014
Mig-6 gene knockout induces neointimal hyperplasia in the vascular smooth muscle cell.
Article in Disease markers, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Single-cell transcriptomics reveals cell-type-specific circadian rhythms and their disruption by acute misalignment in mouse aorta.bioRxiv : the preprint server for biology · 2026Article
- Reduced circulating Mig-6 levels are associated with dysglycemia in metabolic dysfunction associated steatotic liver disease (MASLD).BMJ open diabetes research & care · 2026Article
- Role of Mig-6 in adipose tissue: Implications for glucose metabolism and insulin resistance.PloS one · 2025Article
- ERRFI1 exacerbates hepatic ischemia reperfusion injury by promoting hepatocyte apoptosis and ferroptosis in a GRB2-dependent manner.Molecular medicine (Cambridge, Mass.) · 2024Article
- Exploring shared pathways and the shared biomarker ERRFI1 in Obstructive sleep apnoea and atherosclerosis using integrated bioinformatics analysis.Scientific reports · 2023Article
- Gene 33/Mig6/ERRFI1, an Adapter Protein with Complex Functions in Cell Biology and Human Diseases.Cells · 2021Review
- Mitogen-Inducible Gene 6 Inhibits Angiogenesis by Binding to SHC1 and Suppressing Its Phosphorylation.Frontiers in cell and developmental biology · 2021Article
- An integrated analysis of public genomic data unveils a possible functional mechanism of psoriasis risk via a long-range ERRFI1 enhancer.BMC medical genomics · 2020Article
- The Role of ERRFI1+808T/G Polymorphism in Diabetic Nephropathy.International journal of molecular and cellular medicine · 2019Article
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
Although advances in vascular interventions can reduce the mortality associated with cardiovascular disease, neointimal hyperplasia remains a clinically significant obstacle limiting the success of current interventions. Identification of signaling pathways involved in migration and proliferation of vascular smooth muscle cells (SMCs) is an important approach for the development of modalities to combat this disease. Herein we investigate the role of an immediate early response gene, mitogen-inducible gene-6 (Mig-6), in the development of neointimal hyperplasia using vascular smooth muscle specific Mig-6 knockout mice. We induced endoluminal injury to one side of femoral artery by balloon dilatation in both Mig-6 knockout and control mice. Four weeks following injury, the artery of Mig-6 knockout mice demonstrated a 5.3-fold increase in the neointima/media ratio compared with control mice (P = 0.04). In addition, Mig-6 knockout vascular SMCs displayed an increase in both cell migration and proliferation compared with wild-type SMCs. Taken together, our data suggest that Mig-6 plays a critical role in the development of atherosclerosis. This finding provides new insight into the development of more effective ways to treat and prevent neointimal hyperplasia, particularly in-stent restenosis after percutaneous vascular intervention.
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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.