ArticleCardiovascular research2022
Dynamic changes in chromatin accessibility are associated with the atherogenic transitioning of vascular smooth muscle cells.
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 23 papers.
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Who cites it
23 citing papers in PubMed, 34 citations in OpenAlex.
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- Therapeutic Target Mapping to Advance Drug Repurposing for Cardiovascular Disease: A Perspective from an Explanted Heart Biobank.Journal of personalized medicine · 2026Review
- Inflammation in atherosclerosis: Drivers, mechanisms and therapies.Acta pharmaceutica Sinica. B · 2026Review
- Unraveling Atherosclerosis through Multi-omics: Systematic Insights into the Unique Applications and Clinical Perspectives.Current atherosclerosis reports · 2026Review
- VSMCs and the immune microenvironment: a multidimensional regulatory network driving vascular injury and repair.Frontiers in immunology · 2026Review
- Smooth muscle cells in atherosclerosis: essential but overlooked translational perspectives.European heart journal · 2025Review
- Epigenomic landscape of single vascular cells reflects developmental origin and disease risk loci.Molecular systems biology · 2025Article
- ATF3 Deficiency Exacerbates Ageing-Induced Atherosclerosis and Clinical Intervention Strategy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- The epigenomic landscape of single vascular cells reflects developmental origin and identifies disease risk loci.bioRxiv : the preprint server for biology · 2025Article
- Spatial Gene Expression of Human Coronary Arteries Revealed the Molecular Features of Diffuse Intimal Thickening in Explanted Hearts.International journal of molecular sciences · 2025Article
- Atheroma transcriptomics identifies ARNTL as a smooth muscle cell regulator and with clinical and genetic data improves risk stratification.European heart journal · 2025Article
- Protein swarm-based cause-effect analysis: effects of microRNAs on cooperation networks linking COVID-19 infections, atherosclerosis, and Alzheimer's disease.Frontiers in cardiovascular medicine · 2025Article
- Multiplex Imaging for Cell Phenotyping of Early Human Atherosclerosis.Journal of the American Heart Association · 2024Article
- Network-based prioritization and validation of regulators of vascular smooth muscle cell proliferation in disease.Nature cardiovascular research · 2024Article
- Single-Cell Gene-Regulatory Networks of Advanced Symptomatic Atherosclerosis.Circulation research · 2024Article
- Conditional deletion ofAtherosclerosis plus · 2024Article
- Cholesterol lowering depletes atherosclerotic lesions of smooth muscle cell-derived fibromyocytes and chondromyocytes.Nature cardiovascular research · 2024Article
- Single-Cell RNA Sequencing of Coronary Perivascular Adipose Tissue From End-Stage Heart Failure Patients IdentifiesArteriosclerosis, thrombosis, and vascular biology · 2023Article
- Activating transcription factor 3, glucolipid metabolism, and metabolic diseases.Journal of molecular cell biology · 2023Article
- Role of vascular smooth muscle cell clonality in atherosclerosis.Frontiers in cardiovascular medicine · 2023Review
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Authors and funding
19 authors at 8 institutions in 6 countries.
Funding
Abstract
aimsDe-differentiation and activation of pro-inflammatory pathways are key transitions vascular smooth muscle cells (SMCs) make during atherogenesis. Here, we explored the upstream regulators of this 'atherogenic transition'. METHODS AND
resultsGenome-wide sequencing studies, including Assay for Transposase-Accessible Chromatin using sequencing and RNA-seq, were performed on cells isolated from both murine SMC-lineage-tracing models of atherosclerosis and human atherosclerotic lesions. At the bulk level, alterations in chromatin accessibility were associated with the atherogenic transitioning of lesional SMCs, especially in relation to genes that govern differentiation status and complement-dependent inflammation. Using computational biology, we observed that a transcription factor previously related to coronary artery disease, Activating transcription factor 3 (ATF3), was predicted to be an upstream regulator of genes altered during the transition. At the single-cell level, our results indicated that ATF3 is a key repressor of SMC transitioning towards the subset of cells that promote vascular inflammation by activating the complement cascade. The expression of ATF3 and complement component C3 was negatively correlated in SMCs from human atherosclerotic lesions, suggesting translational relevance. Phenome-wide association studies indicated that genetic variation that results in reduced expression of ATF3 is correlated with an increased risk for atherosclerosis, and the expression of ATF3 was significantly down-regulated in humans with advanced vascular disease.
conclusionOur study indicates that the plasticity of atherosclerotic SMCs may in part be explained by dynamic changes in their chromatin architecture, which in turn may contribute to their maladaptive response to inflammation-induced stress.
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