ArticleThe Biochemical journal2010
Role of cellular bioenergetics in smooth muscle cell proliferation induced by platelet-derived growth factor.
Article in The Biochemical journal, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers.
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Who cites it
83 citing papers in PubMed, 124 citations in OpenAlex.
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- Mitochondrial Calcium Uniporter Regulates Metabolic Remodeling and Smooth Muscle Cell Proliferation in Type 2 Diabetes.Journal of the American Heart Association · 2025Article
- Post-translational modification of transcription factors: perspectives in vascular medicine.Cell death & disease · 2025Review
- The Pathophysiological Role of Vascular Smooth Muscle Cells in Abdominal Aortic Aneurysm.Cells · 2025Review
- MIRO1 controls energy production and proliferation of vascular smooth muscle cells.bioRxiv : the preprint server for biology · 2025Article
- TNFα-mediated subcellular heterogeneity of succinate dehydrogenase activity in human airway smooth muscle cells.American journal of physiology. Lung cellular and molecular physiology · 2025Article
- Mechanisms of metabolic reprogramming in abdominal aortic aneurysm.Frontiers in cell and developmental biology · 2025Review
- Therapeutic Effects of Coenzyme Q10 in the Treatment of Ischemic Stroke.Current nutrition reports · 2024Review
- Heterogeneous distribution of mitochondria and succinate dehydrogenase activity in human airway smooth muscle cells.FASEB bioAdvances · 2024Article
- Vitamin E Attenuates Red-Light-Mediated Vasodilation: The Benefits of a Mild Oxidative Stress.Antioxidants (Basel, Switzerland) · 2024Article
- Dysregulated cellular metabolism in atherosclerosis: mediators and therapeutic opportunities.Nature metabolism · 2024Review
- The role of 6-phosphogluconate dehydrogenase in vascular smooth muscle cell phenotypic switching and angioplasty-induced intimal hyperplasia.JVS-vascular science · 2024Article
- Cellular metabolism changes in atherosclerosis and the impact of comorbidities.Frontiers in cell and developmental biology · 2024Review
- Bioenergetic signatures of neurodevelopmental regression.Frontiers in physiology · 2024Article
- Nanopore long-read RNA sequencing reveals functional alternative splicing variants in human vascular smooth muscle cells.Communications biology · 2023Article
- Cell-Based Measurement of Mitochondrial Function in Human Airway Smooth Muscle Cells.International journal of molecular sciences · 2023Article
- Oncometabolism: A Paradigm for the Metabolic Remodeling of the Failing Heart.International journal of molecular sciences · 2022Review
- Metabolomic Signatures of Autism Spectrum Disorder.Journal of personalized medicine · 2022Article
23 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Abnormal smooth muscle cell proliferation is a hallmark of vascular disease. Although growth factors are known to contribute to cell hyperplasia, the changes in metabolism associated with this response, particularly mitochondrial respiration, remain unclear. Given the increased energy requirements for proliferation, we hypothesized that PDGF (platelet-derived growth factor) would stimulate glycolysis and mitochondrial respiration and that this elevated bioenergetic capacity is required for smooth muscle cell hyperplasia. To test this hypothesis, cell proliferation, glycolytic flux and mitochondrial oxygen consumption were measured after treatment of primary rat aortic VSMCs (vascular smooth muscle cells) with PDGF. PDGF increased basal and maximal rates of glycolytic flux and mitochondrial oxygen consumption; enhancement of these bioenergetic pathways led to a substantial increase in the mitochondrial reserve capacity. Interventions with the PI3K (phosphoinositide 3-kinase) inhibitor LY-294002 or the glycolysis inhibitor 2-deoxy-D-glucose abrogated PDGF-stimulated proliferation and prevented augmentation of glycolysis and mitochondrial reserve capacity. Similarly, when L-glucose was substituted for D-glucose, PDGF-dependent proliferation was abolished, as were changes in glycolysis and mitochondrial respiration. Interestingly, LDH (lactate dehydrogenase) protein levels and activity were significantly increased after PDGF treatment. Moreover, substitution of L-lactate for D-glucose was sufficient to increase mitochondrial reserve capacity and cell proliferation after treatment with PDGF; these effects were inhibited by the LDH inhibitor oxamate. These results suggest that glycolysis, by providing substrates that enhance the mitochondrial reserve capacity, plays an essential role in PDGF-induced cell proliferation, underscoring the integrated metabolic response required for proliferation of VSMCs in the diseased vasculature.
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