ArticlePloS one2014
Sodium tanshinone IIA silate inhibits high glucose-induced vascular smooth muscle cell proliferation and migration through activation of AMP-activated protein kinase.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.
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Who cites it
27 citing papers in PubMed, 1 synthesis or guideline pooled it, 54 citations in OpenAlex.
- A bibliometric analysis of exosomes in aging from 2007 to 2023.Frontiers in medicine · 2024Pooled it
- Unraveling potent therapeutic potentials of tanshinones, lipophilic abietane diterpenes: a holistic literature review.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- Cellular and Molecular Mechanisms of Hyperglycemia-Induced Atherosclerosis and Intervention Strategies of Chinese Herbal Medicine.Drug design, development and therapy · 2026Review
- Vascular smooth muscle cell metabolic reprogramming and phenotypic remodeling in atherosclerosis.Cell death discovery · 2025Review
- Tanshinone I, tanshinone IIA, and cryptotanshinone: key bioactive components modulating vascular smooth muscle cell function.Frontiers in pharmacology · 2025Review
- Tanshinone IIA: a Chinese herbal ingredient for the treatment of atherosclerosis.Frontiers in pharmacology · 2023Review
- Increasing Angiogenesis Factors in Hypoxic Diabetic Wound Conditions by siRNA Delivery: Additive Effect of LbL-Gold Nanocarriers and Desloratadine-Induced Lysosomal Escape.International journal of molecular sciences · 2021Article
- Sodium Tanshinone IIA Silate Exerts Microcirculation Protective Effects against Spinal Cord Injury In Vitro and In Vivo.Oxidative medicine and cellular longevity · 2020Article
- miR‑19a promotes vascular smooth muscle cell proliferation, migration and invasion through regulation of Ras homolog family member B.International journal of molecular medicine · 2019Article
- Sodium tanshinone IIA silate increases melanin synthesis by activating the MAPK and PKA pathways and protects melanocytes from HRSC advances · 2019Article
- Hyperglycemia induces vascular smooth muscle cell dedifferentiation by suppressing insulin receptor substrate-1-mediated p53/KLF4 complex stabilization.The Journal of biological chemistry · 2019Article
- Review
- Danshen Formulae for Cancer: A Systematic Review and Meta-Analysis of High-Quality Randomized Controlled Trials.Evidence-based complementary and alternative medicine : eCAM · 2019Review
- Salvia miltiorrhizaBurge (Danshen): a golden herbal medicine in cardiovascular therapeutics.Acta pharmacologica Sinica · 2018Review
- AMPK activation by Tanshinone IIA protects neuronal cells from oxygen-glucose deprivation.Oncotarget · 2018Article
- The Signaling Pathways Involved in the Antiatherosclerotic Effects Produced by Chinese Herbal Medicines.BioMed research international · 2018Review
- Tanshinone IIA inhibits AGEs-induced proliferation and migration of cultured vascular smooth muscle cells by suppressing ERK1/2 MAPK signaling.Iranian journal of basic medical sciences · 2018Article
- Tanshinone IIA Inhibits Epithelial-Mesenchymal Transition in Bladder Cancer Cells via Modulation of STAT3-CCL2 Signaling.International journal of molecular sciences · 2017Article
- MicroRNAs and metabolic disorders - where are we heading?Archives of medical science : AMS · 2017Article
- Tanshinone IIA ameliorates apoptosis of cardiomyocytes induced by endoplasmic reticulum stress.Experimental biology and medicine (Maywood, N.J.) · 2016Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The proliferation of vascular smooth muscle cells may perform a crucial role in the pathogenesis of diabetic vascular disease. AMPK additionally exerts several salutary effects on vascular function and improves vascular abnormalities. The current study sought to determine whether sodium tanshinone IIA silate (STS) has an inhibitory effect on vascular smooth muscle cell (VSMC) proliferation and migration under high glucose conditions mimicking diabetes without dyslipidemia, and establish the underlying mechanism. In this study, STS promoted the phosphorylation of AMP-activated protein kinase (AMPK) at T172 in VSMCs. VSMC proliferation was enhanced under high glucose (25 mM glucose, HG) versus normal glucose conditions (5.5 mM glucose, NG), and this increase was inhibited significantly by STS treatment. We utilized western blotting analysis to evaluate the effects of STS on cell-cycle regulatory proteins and found that STS increased the expression of p53 and the Cdk inhibitor, p21, subsequent decreased the expression of cell cycle-associated protein, cyclin D1. We further observed that STS arrested cell cycle progression at the G0/G1 phase. Additionally, expression and enzymatic activity of MMP-2, translocation of NF-κB, as well as VSMC migration were suppressed in the presence of STS. Notably, Compound C (CC), a specific inhibitor of AMPK, as well as AMPK siRNA blocked STS-mediated inhibition of VSMC proliferation and migration. We further evaluated its potential for activating AMPK in aortas in animal models of type 2 diabetes and found that Oral administration of STS for 10 days resulted in activation of AMPK in aortas from ob/ob or db/db mice. In conclusion, STS inhibits high glucose-induced VSMC proliferation and migration, possibly through AMPK activation. The growth suppression effect may be attributable to activation of AMPK-p53-p21 signaling, and the inhibitory effect on migration to the AMPK/NF-κB signaling axis.
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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.