ArticleCardiovascular research2022
Drebrin attenuates atherosclerosis by limiting smooth muscle cell transdifferentiation.
Article in Cardiovascular research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 28 citations in OpenAlex.
- Structural mechanisms of drebrin-mediated F-actin network modulation.Nature communications · 2026Article
- Inflammation as a Unifying Axis: Shared Pathogenic Mechanisms in Coronary Atherosclerosis and Chronic Atrophic Gastritis.Journal of inflammation research · 2026Review
- Macrophage-like smooth muscle cells in atherosclerosis.Molecular biology reports · 2025Review
- Review
- Lipid infiltration promotes trans-differentiation of vascular smooth muscle cells into macrophage-like cells in early lesions of human coronary atherosclerosis.Lipids in health and disease · 2025Article
- Vascular Smooth Muscle Cells: A Therapeutic Target in Atherosclerosis.Reviews in cardiovascular medicine · 2025Review
- Overstretch causes lipid accumulation in vascular smooth muscle cells dependent on NADPH oxidase 1.Mechanobiology in medicine · 2025Article
- Aldosterone-Induced Transformation of Vascular Smooth Muscle Cells into Macrophage-like Cells Participates in Inflammatory Vascular Lesions.International journal of molecular sciences · 2025Article
- Disulfidptosis-related gene in acute myocardial infarction and its diagnostic value and functions based on bioinformatics analysis and machine learning.Frontiers in cardiovascular medicine · 2025Article
- Unraveling a Key Molecular Player Governing Pulmonary Alveolar Development.American journal of respiratory cell and molecular biology · 2024Article
- Top Five Stories of the Cellular Landscape and Therapies of Atherosclerosis: Current Knowledge and Future Perspectives.Current medical science · 2024Review
- Proliferation, migration and phenotypic transformation of VSMC induced via Hcy related to up-expression of WWP2 and p-STAT3.PloS one · 2024Article
- Anemoside B4 attenuates abdominal aortic aneurysm by limiting smooth muscle cell transdifferentiation and its mediated inflammation.Frontiers in immunology · 2024Article
- Genetic deletion of MMP12 ameliorates cardiometabolic disease by improving insulin sensitivity, systemic inflammation, and atherosclerotic features in mice.Cardiovascular diabetology · 2023Article
- Targeting oxidative stress as a preventive and therapeutic approach for cardiovascular disease.Journal of translational medicine · 2023Review
- Extracellular traps from activated vascular smooth muscle cells drive the progression of atherosclerosis.Nature communications · 2022Article
- An update on the phenotypic switching of vascular smooth muscle cells in the pathogenesis of atherosclerosis.Cellular and molecular life sciences : CMLS · 2021Review
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
aimsThe F-actin-binding protein Drebrin inhibits smooth muscle cell (SMC) migration, proliferation, and pro-inflammatory signalling. Therefore, we tested the hypothesis that Drebrin constrains atherosclerosis. METHODS AND
resultsSM22-Cre+/Dbnflox/flox/Ldlr-/- (SMC-Dbn-/-/Ldlr-/-) and control mice (SM22-Cre+/Ldlr-/-, Dbnflox/flox/Ldlr-/-, and Ldlr-/-) were fed a western diet for 14-20 weeks. Brachiocephalic arteries of SMC-Dbn -/-/Ldlr-/- mice exhibited 1.5- or 1.8-fold greater cross-sectional lesion area than control mice at 14 or 20 weeks, respectively. Aortic atherosclerotic lesion surface area was 1.2-fold greater in SMC-Dbn-/-/Ldlr-/- mice. SMC-Dbn-/-/Ldlr-/- lesions comprised necrotic cores that were two-fold greater in size than those of control mice. Consistent with their bigger necrotic core size, lesions in SMC-Dbn-/- arteries also showed more transdifferentiation of SMCs to macrophage-like cells: 1.5- to 2.5-fold greater, assessed with BODIPY or with CD68, respectively. In vitro data were concordant: Dbn-/- SMCs had 1.7-fold higher levels of KLF4 and transdifferentiated to macrophage-like cells more readily than Dbnflox/flox SMCs upon cholesterol loading, as evidenced by greater up-regulation of CD68 and galectin-3. Adenovirally mediated Drebrin rescue produced equivalent levels of macrophage-like transdifferentiation in Dbn-/- and Dbnflox/flox SMCs. During early atherogenesis, SMC-Dbn-/-/Ldlr-/- aortas demonstrated 1.6-fold higher levels of reactive oxygen species than control mouse aortas. The 1.8-fold higher levels of Nox1 in Dbn-/- SMCs were reduced to WT levels with KLF4 silencing. Inhibition of Nox1 chemically or with siRNA produced equivalent levels of macrophage-like transdifferentiation in Dbn-/- and Dbnflox/flox SMCs.
conclusionWe conclude that SMC Drebrin limits atherosclerosis by constraining SMC Nox1 activity and SMC transdifferentiation to macrophage-like cells.
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