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| http://dx.doi.org/10.1016/j.jcct.2024.08.003 | DOI Listing |
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Department of Medicine, Division of Cardiovascular Medicine, Stanford University, Stanford, CA, USA.
Vascular sites have distinct susceptibility to atherosclerosis and aneurysm, yet the epigenomic and transcriptomic underpinning of vascular site-specific disease risk is largely unknown. Here, we performed single-cell chromatin accessibility (scATACseq) and gene expression profiling (scRNAseq) of mouse vascular tissue from three vascular sites. Through interrogation of epigenomic enhancers and gene regulatory networks, we discovered key regulatory enhancers to not only be cell type, but vascular site-specific.
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Atherosclerosis, a major cause of cardiovascular diseases, is characterized by the buildup of lipids and chronic inflammation in the arteries, leading to plaque formation and potential rupture. Despite recent advances in single-cell transcriptomics (scRNA-seq), the underlying immune mechanisms and transformations in structural cells driving plaque progression remain incompletely defined. Existing datasets often lack comprehensive coverage and consistent annotations, limiting the utility of downstream analyses.
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CVPath Institute, Gaithersburg, Maryland, USA; University of Maryland, School of Medicine, Baltimore, Maryland, USA. Electronic address:
Background: Effective modification of heavily calcified coronary lesions is critical for successful percutaneous coronary intervention (PCI). Intravascular lithotripsy (IVL), cutting balloons (CBs), and ultra-high-pressure balloons (UHBs) are used commonly, yet data comparing their effectiveness and safety for calcified lesion modification remain unavailable.
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