ArticleCirculation2023
Epigenetic Induction of Smooth Muscle Cell Phenotypic Alterations in Aortic Aneurysms and Dissections.
Article in Circulation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers.
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Who cites it
89 citing papers in PubMed, 124 citations in OpenAlex.
- M1 macrophage-derived exosomal miR-155-5p exacerbates aortic dissection via SMAD5-Mediated regulation of vascular smooth muscle cell phenotype.Bioactive materials · 2026Article
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- Targeted Catalytic Anti-Inflammatory and Antioxidant Therapy for Aortic Dissection Using Biomimetic Nanomaterials.ACS omega · 2026Article
- Genetic and molecular mechanisms of hereditary thoracic aortic aneurysm and dissection (Review).Molecular medicine reports · 2026Review
- The Role of Cysteine-Rich Protein 2 in Aortic Dissection: Implications for VSMC Phenotypic Modulation-CSRP2 Impedes the Progression of Aortic Dissection.Biomolecules · 2026Article
- Emerging roles of the cGAS/STING pathway in cardiovascular diseases.The Journal of clinical investigation · 2026Review
- Integrated Single-Cell and Spatial Analysis Reveals a Metabolic-Immune Axis Driving Aortic Dissection.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- The critical role of the RUNX1/NF-κB transcriptional complex-mediated PVAT-VSMC axis in aortic dissection.Journal of cardiothoracic surgery · 2026Review
- Loss of CASQ2 promotes vascular smooth muscle cell phenotypic switching in aortic dissection uncovered by integrated single-cell transcriptomics.BMC medical genomics · 2026Article
- Piceatannol attenuates thoracic aortic aneurysm progression by targeting STK33.Biology direct · 2026Article
- Single-cell transcriptomics reveals NDRG1/TGF‑β1 associated vascular smooth muscle cell phenotypic switching in chronic thromboembolic pulmonary hypertension.Journal of thrombosis and thrombolysis · 2026Article
- Structural and Signaling Mechanisms of Aortic Wall Failure in Heritable Thoracic Aortic Disease.Cells · 2026Review
- Erosion or Explosion: Integrated Single-Cell Transcriptomics Reveals Cellular Heterogeneity in Aortic Aneurysm and Dissection.Inflammation · 2026Article
- Vascular Aging.Circulation · 2026Review
- Exercise Attenuates Aortic Dissection Via PDE5A-Mediated Inhibition of Vascular Smooth Muscle Cell Phenotypic Switch.Arteriosclerosis, thrombosis, and vascular biology · 2026Article
- SLC1A5 prevents aortic aneurysm and dissection by glutaminolytic-epigenetic orchestration of vascular smooth muscle cell homeostasis.Nature communications · 2026Article
- Article
- The epigenetic and epitranscriptomic regulation of Brd4-Mettl3 axis on STING mediated vascular calcification.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Article
- Aging-AssociatedJournal of the American Heart Association · 2026Article
29 more citing papers are in PubMed but not listed here.
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Authors and funding
15 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundSmooth muscle cell (SMC) phenotypic switching has been increasingly detected in aortic aneurysm and dissection (AAD) tissues. However, the diverse SMC phenotypes in AAD tissues and the mechanisms driving SMC phenotypic alterations remain to be identified.
methodsWe examined the transcriptomic and epigenomic dynamics of aortic SMC phenotypic changes in mice with angiotensin II-induced AAD by using single-cell RNA sequencing and single-cell sequencing assay for transposase-accessible chromatin. SMC phenotypic alteration in aortas from patients with ascending thoracic AAD was examined by using single-cell RNA sequencing analysis.
resultsSingle-cell RNA sequencing analysis revealed that aortic stress induced the transition of SMCs from a primary contractile phenotype to proliferative, extracellular matrix-producing, and inflammatory phenotypes. Lineage tracing showed the complete transformation of SMCs to fibroblasts and macrophages. Single-cell sequencing assay for transposase-accessible chromatin analysis indicated that these phenotypic alterations were controlled by chromatin remodeling marked by the reduced chromatin accessibility of contractile genes and the induced chromatin accessibility of genes involved in proliferation, extracellular matrix, and inflammation. IRF3 (interferon regulatory factor 3), a proinflammatory transcription factor activated by cytosolic DNA, was identified as a key driver of the transition of aortic SMCs from a contractile phenotype to an inflammatory phenotype. In cultured SMCs, cytosolic DNA signaled through its sensor STING (stimulator of interferon genes)-TBK1 (tank-binding kinase 1) to activate IRF3, which bound and recruited EZH2 (enhancer of zeste homolog 2) to contractile genes to induce repressive H3K27me3 modification and gene suppression. In contrast, double-stranded DNA-STING-IRF3 signaling induced inflammatory gene expression in SMCs. In
conclusionsOur study reveals the dynamic epigenetic induction of SMC phenotypic alterations in AAD. DNA damage and cytosolic leakage drive SMCs from a contractile phenotype to an inflammatory phenotype.
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