ArticleJCI insight2018
Smooth muscle glucose metabolism promotes monocyte recruitment and atherosclerosis in a mouse model of metabolic syndrome.
Article in JCI insight, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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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.
The trial behind it
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Who cites it
31 citing papers in PubMed, 44 citations in OpenAlex.
- Histone Lactylation-Mediated Metabolic Remodeling in Vascular Smooth Muscle Cells Aggravates Aortic Aneurysm and Dissection by Promoting Lactate Accumulation.Circulation · 2026Article
- Mitochondrial dysfunction in aortic aneurysm and dissection: mechanisms and therapeutic implications.Frontiers in pharmacology · 2026Review
- Vascular smooth muscle cell metabolic reprogramming and phenotypic remodeling in atherosclerosis.Cell death discovery · 2025Review
- Reprogrammed glucose metabolism in vascular smooth muscle cells and its implications for vascular diseases.Pharmacological research · 2025Review
- The Role and Research Progress of Glycolytic Metabolic Reprogramming in Smooth Muscle Cells in Atherosclerosis.International journal of general medicine · 2025Review
- Glucose transporter 1 in vascular smooth muscle cells is dispensable for abdominal aortic aneurysm induced by angiotensin II.JVS-vascular science · 2025Article
- Insulin receptors in vascular smooth muscle cells regulate plaque stability of atherosclerosis.Cardiovascular research · 2024Article
- Metabolic Responses to Redox Stress in Vascular Cells.Antioxidants & redox signaling · 2024Review
- Glucose metabolism controls monocyte homeostasis and migration but has no impact on atherosclerosis development in mice.Nature communications · 2024Article
- Obese mice have decreased uterine contractility and altered energy metabolism in the uterus at term gestation†.Biology of reproduction · 2024Article
- GPR40/GPR120 Agonist GW9508 Improves Metabolic Syndrome-Exacerbated Periodontitis in Mice.International journal of molecular sciences · 2024Article
- Identification of plasma miR-4505, miR-4743-5p and miR-4750-3p as novel diagnostic biomarkers for coronary artery disease in patients with type 2 diabetes mellitus: a case-control study.Cardiovascular diabetology · 2024Article
- Fluoride impairs vascular smooth muscle A7R5 cell lines via disrupting amino acids metabolism.Journal of translational medicine · 2024Article
- Dysregulated cellular metabolism in atherosclerosis: mediators and therapeutic opportunities.Nature metabolism · 2024Review
- VNS improves VSMC metabolism and arteriogenesis in infarcted hearts through m/n-AChR-Akt-SDF-1α in adult male rats.Journal of molecular histology · 2024Article
- Cellular metabolism changes in atherosclerosis and the impact of comorbidities.Frontiers in cell and developmental biology · 2024Review
- miR-3529-3p/ABCA1 axis regulates smooth muscle cell homeostasis by enhancing inflammation via JAK2/STAT3 pathway.Frontiers in cardiovascular medicine · 2024Article
- Bacterial indole-3-lactic acid affects epithelium-macrophage crosstalk to regulate intestinal homeostasis.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- GPR40 deficiency worsens metabolic syndrome-associated periodontitis in mice.Journal of periodontal research · 2023Article
- The Therapeutic Strategies Targeting Mitochondrial Metabolism in Cardiovascular Disease.Pharmaceutics · 2022Review
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
Abstract
Metabolic syndrome contributes to cardiovascular disease partly through systemic risk factors. However, local processes in the artery wall are becoming increasingly recognized to exacerbate atherosclerosis both in mice and humans. We show that arterial smooth muscle cell (SMC) glucose metabolism markedly synergizes with metabolic syndrome in accelerating atherosclerosis progression, using a low-density lipoprotein receptor-deficient mouse model. SMCs in proximity to atherosclerotic lesions express increased levels of the glucose transporter GLUT1. Cytokines, such as TNF-α produced by lesioned arteries, promote GLUT1 expression in SMCs, which in turn increases expression of the chemokine CCL2 through increased glycolysis and the polyol pathway. Furthermore, overexpression of GLUT1 in SMCs, but not in myeloid cells, accelerates development of larger, more advanced lesions in a mouse model of metabolic syndrome, which also exhibits elevated levels of circulating Ly6Chi monocytes expressing the CCL2 receptor CCR2. Accordingly, monocyte tracing experiments demonstrate that targeted SMC GLUT1 overexpression promotes Ly6Chi monocyte recruitment to lesions. Strikingly, SMC-targeted GLUT1 overexpression fails to accelerate atherosclerosis in mice that do not exhibit the metabolic syndrome phenotype or monocytosis. These results reveal a potentially novel mechanism whereby arterial smooth muscle glucose metabolism synergizes with metabolic syndrome to accelerate monocyte recruitment and atherosclerosis progression.
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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.