ArticleVascular pharmacology2016
Increased aerobic glycolysis is important for the motility of activated VSMC and inhibited by indirubin-3'-monoxime.
Article in Vascular pharmacology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 58 citations in OpenAlex.
- Energetic Decoding of VSMC Plasticity: Metabolic Reprogramming and Phenotypic Switching.Cardiovascular drugs and therapy · 2026Review
- Review
- Role of vascular smooth muscle cell pathobiology in sepsis‑induced vasoplegia (Review).International journal of molecular medicine · 2026Review
- Reprogrammed glucose metabolism in vascular smooth muscle cells and its implications for vascular diseases.Pharmacological research · 2025Review
- Inhibition of vascular intimal hyperplasia by the myokine Musclin: the role of NPR3/raptor/mTORC1-mediated glycolysis and phenotypic switching of VSMCs.Acta biochimica et biophysica Sinica · 2025Article
- Vascular Smooth Muscle Cell Metabolic Reprogramming in Arteriovenous Fistula Failure.Biomedicines · 2025Review
- Hepatic antioxidant capacity, immune response, and glycolysis of Tibetan sheep in response to dietary soluble protein levels.Protoplasma · 2025Article
- A review of the link between the lactate-GPR81 axis and mitochondrial angiopathy in MELAS based on imaging characteristics.Journal of neurology · 2025Review
- Proteomic profiling reveals a higher presence of glycolytic enzymes in human atherosclerotic lesions with unfavourable histological characteristics.Cardiovascular research · 2025Article
- Cathepsin D inhibits AGEs-induced phenotypic transformation in vascular smooth muscle cells.Scientific reports · 2025Article
- The Role and Research Progress of Glycolytic Metabolic Reprogramming in Smooth Muscle Cells in Atherosclerosis.International journal of general medicine · 2025Review
- Regulation of osteogenic differentiation in vascular smooth muscle cells under high-glucose condition.Frontiers in endocrinology · 2025Review
- Stress, Vascular Smooth Muscle Cell Phenotype and Atherosclerosis: Novel Insight into Smooth Muscle Cell Phenotypic Transition in Atherosclerosis.Current atherosclerosis reports · 2024Review
- Fluoride impairs vascular smooth muscle A7R5 cell lines via disrupting amino acids metabolism.Journal of translational medicine · 2024Article
- Targeting glycolytic pathway in fibroblast-like synoviocytes for rheumatoid arthritis therapy: challenges and opportunities.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023Review
- Role of glycolysis in diabetic atherosclerosis.World journal of diabetes · 2023Review
- Current understanding of the contribution of lactate to the cardiovascular system and its therapeutic relevance.Frontiers in endocrinology · 2023Article
- Oncometabolism: A Paradigm for the Metabolic Remodeling of the Failing Heart.International journal of molecular sciences · 2022Review
- Phenotypic plasticity of vascular smooth muscle cells in vascular calcification: Role of mitochondria.Frontiers in cardiovascular medicine · 2022Review
- Glucose consumption of vascular cell types in culture: toward optimization of experimental conditions.American journal of physiology. Cell physiology · 2022Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Increased aerobic glycolysis is a recognized feature of multiple cellular phenotypes and offers a potential point for drug interference, as pursued by anti-tumor agents targeting the Warburg effect. This study aimed at examining the role of aerobic glycolysis for migration of vascular smooth muscle cells (VSMC) and its susceptibility to the small molecule indirubin-3'-monoxime (I3MO). Activation of VSMC with platelet-derived growth factor (PDGF) resulted in migration and increased glycolytic activity which was accompanied by an increased glucose uptake and hexokinase (HK) 2 expression. Inhibition of glycolysis or hexokinase by pharmacological agents or siRNA-mediated knockdown significantly reduced the migratory behavior in VSMC without affecting cell viability or early actin cytoskeleton rearrangement. I3MO, previously recognized as inhibitor of VSMC migration, was able to counteract the PDGF-activated increase in glycolysis and HK2 abundance. Activation of signal transducer and activator of transcription (STAT) 3 could be identified as crucial event in upregulation of HK2 and glycolytic activity in PDGF-stimulated VSMC and as point of interference for I3MO. I3MO did not inhibit hypoxia-inducible factor (HIF)1α-dependent transcription nor influence miRNA 143 levels, other potential regulators of HK2 levels. Overall, we demonstrate that increased aerobic glycolysis is an important factor for the motility of activated VSMC and that the anti-migratory property of I3MO may partly depend on impairment of glycolysis via a compromised STAT3/HK2 signaling axis.
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Registered trials
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