ArticleScientific reports2017
FAM3B mediates high glucose-induced vascular smooth muscle cell proliferation and migration via inhibition of miR-322-5p.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 30 citations in OpenAlex.
- The Ratio of Red Blood Cell Distribution Width To Serum Albumin and its Association with Cardiovascular and All-Cause Mortality Risk in Diabetic Patients: A Cohort Study Using NHANES Data from 1999 to 2018.High blood pressure & cardiovascular prevention : the official journal of the Italian Society of Hypertension · 2025Article
- Article
- Citropten Inhibits Vascular Smooth Muscle Cell Proliferation and Migration via the TRPV1 Receptor.ACS omega · 2024Article
- Derivation of a Protein Risk Score for Cardiovascular Disease Among a Multiracial and Multiethnic HIV+ Cohort.Journal of the American Heart Association · 2023Article
- MicroRNAs as Biomarkers for Coronary Artery Disease Related to Type 2 Diabetes Mellitus-From Pathogenesis to Potential Clinical Application.International journal of molecular sciences · 2022Review
- Dexamethasone suppresses the proliferation and migration of VSMCs by FAK in high glucose conditions.BMC pharmacology & toxicology · 2022Article
- Focal adhesion kinase-related pathways may be suppressed by metformin in vascular smooth muscle cells in high glucose conditions.Endocrinology, diabetes & metabolism · 2022Article
- DR1 Activation Inhibits the Proliferation of Vascular Smooth Muscle Cells through Increasing Endogenous HAging and disease · 2022Article
- Upregulation of TGF-β type II receptor in high glucose-induced vascular smooth muscle cells.Molecular biology reports · 2022Article
- Identifying potential therapeutic targets of Tang-Yi-Ping for the treatment of impaired glucose tolerance: a tandem mass tag-labeled quantitative proteomic analysis.Annals of translational medicine · 2021Article
- MicroRNA-342-5p activates the Akt signaling pathway by downregulating PIK3R1 to modify the proliferation and differentiation of vascular smooth muscle cells.Experimental and therapeutic medicine · 2020Article
- Inhibition of Notch Signaling Alleviated Diabetic Macrovasculopathy in an In Vitro Model.Acta Cardiologica Sinica · 2020Article
- Retinal Physiology and Circulation: Effect of Diabetes.Comprehensive Physiology · 2020Review
- Fetal malnutrition-induced catch up failure is caused by elevated levels of miR-322 in rats.Scientific reports · 2020Article
- MiR-15b and miR-322 inhibit SETD3 expression to repress muscle cell differentiation.Cell death & disease · 2019Article
- High glucose promotes vascular smooth muscle cell proliferation by upregulating proto-oncogene serine/threonine-protein kinase Pim-1 expression.Oncotarget · 2017Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The proliferation and migration of vascular smooth muscle cells (VSMCs) play an essential role during the development of cardiovascular diseases (CVDs). While many factors potentially contribute to the abnormal activation of VSMCs, hyperglycemia is generally believed to be a major causative factor. On the other hand, FAM3B (named PANDER for its secretory form) is a uniquely structured protein strongly expressed within and secreted from the endocrine pancreas. FAM3B is co-secreted with insulin from the β-cell upon glucose stimulation and regulates glucose homeostasis. In the present study, we sought to determine the roles of FAM3B in the regulation of VSMC physiology, especially under the hyperglycemic condition. We found that FAM3B expression was induced by hyperglycemia both in vivo and in vitro. FAM3B knockdown inhibited, whereas FAM3B overexpression accelerated VSMC proliferation and migration. At the molecular level, FAM3B inhibited miR-322-5p expression, and enforced expression of miR-322-5p antagonized FAM3B-induced VSMC proliferation and migration, suggesting that FAM3B facilitated VSMC pathological activation via miR-322-5p. Taken together, FAM3B mediates high glucose-induced VSMC proliferation and migration via inhibition of miR-322-5p. Thus, FAM3B may therefore serve as a novel therapeutic target for diabetes-related CVDs.
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