ArticleNature cardiovascular research2024
Cholesterol lowering depletes atherosclerotic lesions of smooth muscle cell-derived fibromyocytes and chondromyocytes.
Article in Nature cardiovascular research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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
18 citing papers in PubMed.
- Cell-Surface Signatures and Targets of Modulated Vascular Smooth Muscle Cells in Atherosclerosis: From State Identification to Precision Intervention.Journal of cardiovascular development and disease · 2026Review
- Loss of the Coronary Artery Disease Risk GeneCirculation · 2026Article
- Fibroblast-like cells accumulate late in human coronary atherosclerosis contributing to necrotic core formation.Cardiovascular research · 2026Article
- HDL Regulates TGFβ-Receptor Lipid Raft Partitioning, Restoring Contractile Features of Cholesterol-Loaded Vascular Smooth Muscle Cells.JACC. Basic to translational science · 2026Article
- Single-Cell Multimodal Profiling Highlights Persistent Aortic Smooth Muscle Cell Changes in Diabetic Mice Despite Glycemic Control.Arteriosclerosis, thrombosis, and vascular biology · 2026Article
- Coronary atherosclerotic plaque composition and classification in hypercholesterolemic pigs.Atherosclerosis · 2026Article
- Progression of Established Atherosclerotic Lesions Is Not Inhibited by Endothelial Knockout of Caveolin-1-Brief Report.Arteriosclerosis, thrombosis, and vascular biology · 2026Article
- Targeting modulated vascular smooth muscle cells in atherosclerosis via FAP-directed immunotherapy.Science (New York, N.Y.) · 2026Article
- Review
- Vascular smooth muscle cell metabolic reprogramming and phenotypic remodeling in atherosclerosis.Cell death discovery · 2025Review
- Plasminogen activator inhibitor 1 promotes aortic aging-like pathophysiology in humans and mice.The Journal of clinical investigation · 2025Article
- YAP/TAZ deletion in vascular smooth muscle cells mirrors atherosclerosis-associated transcriptional programs.Journal of molecular and cellular cardiology plus · 2025Article
- Smooth muscle cells in atherosclerosis: essential but overlooked translational perspectives.European heart journal · 2025Review
- Mapping atherogenesis mechanisms in smooth muscle cells by targeting genes linked to coronary artery disease.iScience · 2025Article
- Delineation of a thrombin receptor-stimulated vascular smooth muscle cell transition generating cells in the plaque-stabilizing fibrous cap.Cardiovascular research · 2025Article
- Smooth Muscle Cell-Derived Fibronectin Promotes an Atheroprotective Smooth Muscle Cell Phenotype Associated With Altered NO-cGMP Signaling.Journal of the American Heart Association · 2025Article
- Hypercholesterolemia-induced LXR signaling in smooth muscle cells contributes to vascular lesion remodeling and visceral function.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Chronic inflammation and vascular cell plasticity in atherosclerosis.Nature cardiovascular research · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors.
Funding
Abstract
Drugs that lower plasma apolipoprotein B (ApoB)-containing lipoproteins are central to treating advanced atherosclerosis and provide partial protection against clinical events. Previous research showed that lowering ApoB-containing lipoproteins stops plaque inflammation, but how these drugs affect the heterogeneous population of plaque cells derived from smooth muscle cells (SMCs) is unknown. SMC-derived cells are the main cellular component of atherosclerotic lesions and the source of structural components that determine the size of plaques and their propensity to rupture and trigger thrombosis, the proximate cause of heart attack and stroke. Using lineage tracing and single-cell techniques to investigate the full SMC-derived cellular compartment in progressing and regressing plaques in mice, here we show that lowering ApoB-containing lipoproteins reduces nuclear factor kappa-light-chain-enhancer of activated B cells signaling in SMC-derived fibromyocytes and chondromyocytes and leads to depletion of these abundant cell types from plaques. These results uncover an important mechanism through which cholesterol-lowering drugs can achieve plaque regression.
Indexed as
Identifiers
39196190What 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.