ReviewHeliyon2024
Vascular smooth muscle cell phenotypic switching in atherosclerosis.
Review in Heliyon, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
45 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Pooled it
- Pathophysiology of Atherosclerotic Carotid Disease.Seminars in neurology · 2026Review
- FOXC1: A Key Transcription Factor of VSMC-Derived Foam Cell Formation in Atherosclerotic Plaque Instability.The Kaohsiung journal of medical sciences · 2026Article
- Review
- Integration of Three-Dimensional Cell Culture Techniques and Photobiomodulation for Supportive Differentiation of Adipose-Derived Stem Cells into Smooth Muscle.Cell biochemistry and function · 2026Review
- Integrated single-cell and spatial transcriptomics reveal stromal-immune-vascular crosstalk in patients with interstitial cystitis/bladder pain syndrome.Experimental & molecular medicine · 2026Article
- Review
- Research Progress on the Molecular Mechanism of LRP1 and TGFβ-PDGFRβ Signaling Network in Atherosclerosis and Vascular Remodeling.International journal of molecular sciences · 2026Review
- Inflammatory Neovascularization and Vascular Remodeling Associated With Carotid Plaque Destabilization.CNS neuroscience & therapeutics · 2026Article
- Pharmacogenomics of Atherosclerotic Plaque: Pathophysiological Background and Therapeutic Perspectives.Current atherosclerosis reports · 2026Review
- LRG1 as a Potential Therapeutic Target in Atherosclerosis: Mechanistic Basis and Current Evidence.Cells · 2026Review
- Immune-Checkpoint-Inhibitor-Related Cardiovascular Toxicities in Cancer: A Mechanistic Review of Molecular Pathways with AI-Assisted Literature Clustering.International journal of molecular sciences · 2026Review
- Atherosclerotic Plaque Characterization Magnetic Resonance Imaging In Vitro at 1.5 Tesla for the Assessment of Coronary Artery Disease.Journal of clinical medicine · 2026Article
- From Byproduct to Regulator: The Expanding Role of Lactate and Lactylation in Cardiovascular Physiology and Disease.Biology · 2026Review
- Re-analysis of single-cell transcriptomics reveals a critical role of TNS1 gene in driving contractile VSMC transdifferentiation into macrophage-like SMC and atherosclerotic plaque instability.Clinical and translational medicine · 2026Article
- Oxidative Stress-Induced DNA Damage Response Pathways in Aortic Disease: Implications for Inflammation and Vascular Degeneration.International journal of molecular sciences · 2026Review
- Vascular Smooth Muscle-Specific NLRP3 Hyperactivation Drives Arterial Intimal Hyperplasia in Mice.Research square · 2026Article
- Ameliorative effects of tallow and olive oil on hyperlipidemia-induced atherogenesis in male albino rats.Scientific reports · 2026Article
- Phosphomimetic Thrombospondin-1 Modulates Integrin β1-FAK Signaling and Vascular Cell Functions.Biomolecules · 2026Article
- Trained Immunity-Like Memory in Vascular Structural Cells: Metabolic-Epigenetic Reprogramming as a Driving Mechanism of Atherosclerosis and Residual Cardiovascular Risk.Journal of inflammation research · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Atherosclerosis (AS) is a complex pathology process involving intricate interactions among various cells and biological processes. Vascular smooth muscle cells (VSMCs) are the predominant cell type in normal arteries, and under atherosclerotic stimuli, VSMCs respond to altered blood flow and microenvironment changes by downregulating contractile markers and switching their phenotype. This review overviews the diverse phenotypes of VSMCs, including the canonical contractile VSMCs, synthetic VSMCs, and phenotypes resembling macrophages, foam cells, myofibroblasts, osteoblasts/chondrocytes, and mesenchymal stem cells. We summarize their presumed protective and pro-atherosclerotic roles in AS development. Additionally, we underscore the molecular mechanisms and regulatory pathways governing VSMC phenotypic switching, encompassing transcriptional regulation, biochemical factors, plaque microenvironment, epigenetics, miRNAs, and the cytoskeleton, emphasizing their significance in AS development. Finally, we outline probable future research directions targeting VSMCs, offering insights into potential therapeutic strategies for AS management.
Indexed as
Identifiers
What Socratic holds
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 Socratic graph.