ArticleScientific reports2018
Notoginsenoside R1 inhibits vascular smooth muscle cell proliferation, migration and neointimal hyperplasia through PI3K/Akt signaling.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 48 citations in OpenAlex.
- Research progress on the mechanism of panax notoginseng saponin in the treatment of atherosclerosis.Frontiers in cardiovascular medicine · 2026Review
- Cell migration in diabetic wound healing: Molecular mechanisms and therapeutic strategies (Review).International journal of molecular medicine · 2025Review
- The effect of panax ginseng on intimal hyperplasia in rats with abdominal aortic intimal injury.Turk gogus kalp damar cerrahisi dergisi · 2025Article
- The role of Nrf2 signaling pathway in diabetic cardiomyopathy: from pathogenesis to traditional Chinese medicine interventions.Frontiers in cardiovascular medicine · 2025Review
- Article
- Review
- Investigation of Ginseng-Ophiopogon Injection on Enhancing Physical Function by Pharmacogenomics and Metabolomics Evaluation.Combinatorial chemistry & high throughput screening · 2024Article
- Cellular mechanotransduction in health and diseases: from molecular mechanism to therapeutic targets.Signal transduction and targeted therapy · 2023Review
- Notoginsenoside R1 Promotes Migration, Adhesin, Spreading, and Osteogenic Differentiation of Human Adipose Tissue-Derived Mesenchymal Stromal Cells.Molecules (Basel, Switzerland) · 2022Article
- Anemoside B4 Inhibits Vascular Smooth Muscle Cell Proliferation, Migration, and Neointimal Hyperplasia.Frontiers in cardiovascular medicine · 2022Article
- Mechanisms and Efficacy of Traditional Chinese Medicine in Heart Failure.Frontiers in pharmacology · 2022Review
- Hydroxysafflor Yellow A inhibits the viability and migration of vascular smooth muscle cells induced by serum from rats with chronic renal failure via inactivation of the PI3K/Akt signaling pathway.Experimental and therapeutic medicine · 2021Article
- Pathological Change and Whole Transcriptome Alternation Caused by ePTFE Implantation in Myocardium.BioMed research international · 2021Article
- Genetic Regulation of Atherosclerosis-Relevant Phenotypes in Human Vascular Smooth Muscle Cells.Circulation research · 2020Article
- 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
- Metabolomes and transcriptomes revealed the saponin distribution in root tissues ofJournal of ginseng research · 2020Article
- Inhibition of ERK or Akt ameliorates intimal hyperplasia via up-regulation of Cx37 and down-regulation of Cx43 in balloon injury rat model.Cardiovascular diagnosis and therapy · 2020Article
- Focus on Notoginsenoside R1 in Metabolism and Prevention Against Human Diseases.Drug design, development and therapy · 2020Review
- Knockdown of GC binding factor 2 by RNA interference inhibits invasion and migration of vascular smooth muscle cells.Molecular medicine reports · 2019Article
- Notoginsenoside R1 (NGR1) Attenuates Chronic Atrophic Gastritis in Rats.Medical science monitor : international medical journal of experimental and clinical research · 2019Article
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Authors and funding
8 authors at 3 institutions in 3 countries.
Funding
Abstract
Restenosis caused by neointimal hyperplasia significantly decreases long-term efficacy of percutaneous transluminal angioplasty (PTA), stenting, and by-pass surgery for managing coronary and peripheral arterial diseases. A major cause of pathological neointima formation is abnormal vascular smooth muscle cell (VSMC) proliferation and migration. Notoginsenoside R1 (NGR1) is a novel saponin that is derived from Panax notoginseng and has reported cardioprotective, neuroprotective and anti-inflammatory effects. However, its role in modulating VSMC neointima formation remains unexplored. Herein, we report that NGR1 inhibits serum-induced VSMC proliferation and migration by regulating VSMC actin cytoskeleton dynamics. Using a mouse femoral artery endothelium denudation model, we further demonstrate that systemic administration of NGR1 had a potent therapeutic effect in mice, significantly reducing neointimal hyperplasia following acute vessel injury. Mechanistically, we show that NGR1's mode of action is through inhibiting the activation of phosphatidylinositol 3-kinase (PI3K)/Akt signaling. Taken together, this study identified NGR1 as a potential therapeutic agent for combating restenosis after PTA in cardiovascular diseases.
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