ArticleInternational journal of molecular medicine2018
Metformin-induced activation of AMPK inhibits the proliferation and migration of human aortic smooth muscle cells through upregulation of p53 and IFI16.
Article in International journal of molecular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 22 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
22 citing papers in PubMed, 1 synthesis or guideline pooled it, 45 citations in OpenAlex.
- Effect of Intensive Glycemic Control on Myocardial Infarction Outcome in Patients with Type 2 Diabetes Mellitus: A Systematic Review and Meta-Analysis.Journal of diabetes research · 2023Pooled it
- Insights into targeting LKB1 in tumorigenesis.Genes & diseases · 2025Review
- DNA sensors in metabolic and cardiovascular diseases: Molecular mechanisms and therapeutic prospects.Immunological reviews · 2025Review
- The IPBiochimica et biophysica acta. Molecular basis of disease · 2025Article
- LKB1 biology: assessing the therapeutic relevancy of LKB1 inhibitors.Cell communication and signaling : CCS · 2024Review
- Anxiolytic effect of antidiabetic metformin is mediated by AMPK activation in mPFC inhibitory neurons.Molecular psychiatry · 2023Article
- AMPK Activation Restores Salivary Function Following Radiation Treatment.Journal of dental research · 2023Article
- From Diabetes to Atherosclerosis: Potential of Metformin for Management of Cardiovascular Disease.International journal of molecular sciences · 2022Review
- Potential Effects of Metformin on the Vitality, Invasion, and Migration of Human Vascular Smooth Muscle Cells via Downregulating lncRNA-ATB.Disease markers · 2022Article
- Graphene oxide exacerbates dextran sodium sulfate-induced colitis via ROS/AMPK/p53 signaling to mediate apoptosis.Journal of nanobiotechnology · 2021Article
- Metformin alleviates β-glycerophosphate-induced calcification of vascular smooth muscle cells via AMPK/mTOR-activated autophagy.Experimental and therapeutic medicine · 2021Article
- Can Metformin Exert as an Active Drug on Endothelial Dysfunction in Diabetic Subjects?Biomedicines · 2020Review
- TIM‑3 inhibits PDGF‑BB‑induced atherogenic responses in human artery vascular smooth muscle cells.Molecular medicine reports · 2020Article
- Investigating the Vascular Toxicity Outcomes of the Irreversible Proteasome Inhibitor Carfilzomib.International journal of molecular sciences · 2020Article
- Metformin decreases hyaluronan synthesis by vascular smooth muscle cells.Journal of investigative medicine : the official publication of the American Federation for Clinical Research · 2020Article
- Probe into the Target and Mechanism of Jianpi Xiaoke Prescription for Treating Type 2 Diabetes Mellitus through miRNA Expression Profiling.Evidence-based complementary and alternative medicine : eCAM · 2020Article
- Metformin and Vascular Diseases: A Focused Review on Smooth Muscle Cell Function.Frontiers in pharmacology · 2020Review
- Long Noncoding RNABioMed research international · 2020Article
- Pleiotropic Activity of Metformin and Its Sulfonamide Derivatives on Vascular and Platelet Haemostasis.Molecules (Basel, Switzerland) · 2019Article
- [Metformin inhibits aortic atherosclerosis in mice by regulating actin skeleton in vascular smooth muscle cells].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2019Article
Corrections and comments
- Retracted
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The proliferation and migration of vascular smooth muscle cells are significant in the development and progression of atherosclerosis and plaque rupture. Metformin is a widely used antidiabetic drug, which has been reported to inhibit cell growth and migration. The antiproliferative and antimigratory effects of metformin have been attributed to 5' adenosine monophosphate-activated protein kinase (AMPK) activation. The purpose of the present study was to investigate the effects of metformin on primary human aortic muscle cells (HASMCs) in vitro and to clarify the underlying mechanism. We investigated the effectiveness of metformin in inhibiting the proliferation and migration of HASMCs in vitro using RNA extraction and reverse transcription-quantitative polymerase chain reaction (RT-qPCR), cell number counting, cell viability assay, cell cycle assay and cell migration assay. Through transfection with small interfering (si)RNA targeting p53 and interferon‑inducible protein 16 (IFI16), the roles of p53 and IFI16 in these processes were evaluated. The present study demonstrated that p53, IFI16 and AMPK were upregulated in senescent primary HASMCs, which exhibited a decrease in proliferation and migration. In addition, metformin was able to activate p53, IFI16 and AMPK, in order to inhibit proliferation and migration of HASMCs. Furthermore, siRNA‑mediated knockdown of p53 and IFI16 attenuated AMPK activation and reversed the suppressive effects of metformin. Notably, in response to metformin, the activation of AMPK was not observed in p53‑ and IFI16‑silenced HASMCs. These results indicated that metformin-induced activation of AMPK suppresses the proliferation and migration of HASMCs by upregulating p53 and IFI16. These findings suggested that metformin may have potential use in the treatment of atherosclerosis.
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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.