ArticleDiabetologia2017
SHP-1 activation inhibits vascular smooth muscle cell proliferation and intimal hyperplasia in a rodent model of insulin resistance and diabetes.
Article in Diabetologia, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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15 citing papers in PubMed, 30 citations in OpenAlex.
- Construction of the ceRNA Regulatory Network Associated with Milk Fat Metabolism.Animals : an open access journal from MDPI · 2026Article
- C/EBPβ-Lin28a positive feedback loop triggered by C/EBPβ hypomethylation enhances the proliferation and migration of vascular smooth muscle cells in restenosis.Chinese medical journal · 2025Article
- Platelet Membrane-Encapsulated Poly(lactic-International journal of pharmaceutics: X · 2024Article
- Association between triglyceride-glucose index and all-cause mortality in patients underwent transcatheter aortic valve replacement.BMC cardiovascular disorders · 2024Article
- PTPN14 aggravates neointimal hyperplasia via boosting PDGFRβ signaling in smooth muscle cells.Nature communications · 2024Article
- CDKN2B-AS1 mediates proliferation and migration of vascular smooth muscle cells induced by insulin.Cell and tissue research · 2023Article
- The preoperative triglyceride-glucose index has a positive effect on predicting the risk of short-term restenosis after carotid artery stenting: a retrospective cohort study.Frontiers in neurology · 2023Article
- Icariside II Restores Vascular Smooth Muscle Cell Contractile Phenotype by Enhancing the Focal Adhesion Signaling Pathway in the Rat Vascular Remodeling Model.Frontiers in pharmacology · 2022Article
- Pathogenesis and Clinical Significance of In-Stent Restenosis in Patients with Diabetes.International journal of environmental research and public health · 2021Review
- Insulin's actions on vascular tissues: Physiological effects and pathophysiological contributions to vascular complications of diabetes.Molecular metabolism · 2021Review
- Vitamin D3-VDR-PTPN6 axis mediated autophagy contributes to the inhibition of macrophage foam cell formation.Autophagy · 2021Article
- Triglyceride-glucose index is associated with in-stent restenosis in patients with acute coronary syndrome after percutaneous coronary intervention with drug-eluting stents.Cardiovascular diabetology · 2021Observational
- Targeting the epigenome in in-stent restenosis: from mechanisms to therapy.Molecular therapy. Nucleic acids · 2021Review
- Homozygous receptors for insulin and not IGF-1 accelerate intimal hyperplasia in insulin resistance and diabetes.Nature communications · 2019Article
- Platelet-derived miR-223 promotes a phenotypic switch in arterial injury repair.The Journal of clinical investigation · 2019Article
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Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
Abstract
aims/hypothesisAccelerated migration and proliferation of vascular smooth muscle cells (VSMCs) enhances arterial restenosis after angioplasty in insulin resistance and diabetes. Elevation of Src homology 2-containing protein tyrosine phosphatase 1 (SHP-1) induces apoptosis in the microvasculature. However, the role of SHP-1 in intimal hyperplasia and restenosis has not been clarified in insulin resistance and diabetes.
methodsWe used a femoral artery wire injury mouse model, rodent models with insulin resistance and diabetes, and patients with type 2 diabetes. Further, we modulated SHP-1 expression using a transgenic mouse that overexpresses SHP-1 in VSMCs (Shp-1-Tg). SHP-1 agonists were also employed to study the molecular mechanisms underlying the regulation of SHP-1 by oxidised lipids.
resultsMice fed a high-fat diet (HFD) exhibited increased femoral artery intimal hyperplasia and decreased arterial SHP-1 expression compared with mice fed a regular diet. Arterial SHP-1 expression was also decreased in Zucker fatty rats, Zucker diabetic fatty rats and in patients with type 2 diabetes. In primary cultured VSMCs, oxidised LDL suppressed SHP-1 expression by activating Mek-1 (also known as Map2k1) and increased DNA methylation of the Shp-1 promoter. VSMCs from Shp-1-Tg mice exhibited impaired platelet-derived growth factor (PDGF)-stimulated tyrosine phosphorylation with a concomitant decrease in PDGF-stimulated VSMC proliferation and migration. Similarly, HFD-fed Shp-1-Tg mice and mice treated with the SHP-1 inducer, Icariside II, were protected from the development of intimal hyperplasia following wire injury. CONCLUSIONS/
interpretationSuppression of SHP-1 by oxidised lipids may contribute to the excessive VSMC proliferation, inflammatory cytokine production and intimal hyperplasia observed in arteries from diabetes and insulin resistance. Augmenting SHP-1 levels is a potential therapeutic strategy to maintain stent patency in patients with insulin resistance and diabetes.
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