Atherosclerosis and Cardiovascular Diseases

The paper identifies novel autophagy and immunoregulatory genes and pathways in PAD plaques through transcriptomic analysis of paired atheromatous and control vessel tissues.

This study maps the qualitative changes in coronary atherosclerotic cap characteristics during lesion progression and destabilization using a pseudo-timeline approach.

This study shows that Saa3 deficiency reduces atherosclerosis in mice by altering aortic immune cell composition and function.

The paper shows that the anti-nucleolin aptamer iSN04 inhibits vascular smooth muscle cell proliferation and promotes differentiation, suggesting it as a potential therapy for vascular disease.

The paper identifies CD200 as a specific marker for vascular smooth muscle cells and their derived cells in atherosclerosis using CITE-seq and validates it across multiple techniques.

The paper develops an integrated preclinical atherosclerosis database by extracting data from mouse models and provides tools for standardized analysis and integration with transcriptomics software.

The paper uses multimodal single-cell profiling to identify diverse monocyte subtypes and links them to cardiovascular disease risk factors.

This study shows that oleic acid pre-exposure rewires CD4+ T cell metabolism, promoting pro-inflammatory differentiation upon activation.

The paper integrates single-cell RNA-seq and spatial transcriptomics data to reveal cellular interactions and changes in human atherosclerosis.

This study performs a meta-analysis of scRNA-seq datasets to map human atherosclerosis cell diversity and identifies disease-relevant vascular cell states and markers.

The paper identifies a novel macrophage subpopulation, lipid-handling macrophages, that is enriched with CAD genetic risk and shows how a risk variant affects FDX1 through AP-1 and C/EBP-beta recruitment.

This study shows that CypD promotes macrophage apoptosis and necrotic core formation in atherosclerosis by affecting mitochondrial function and inflammation.

The paper identifies sex-stratified gene regulatory networks in atherosclerotic plaques, showing female plaques are enriched with myofibroblast-like smooth muscle cell networks.

The paper identifies dysregulated metabolic pathways in vascular smooth muscle cells during phenotypic switching and links them to atherosclerosis.

This paper identifies INKILN, a human-specific lncRNA that promotes vascular smooth muscle inflammation by stabilizing MKL1 and interacting with USP10.

This study profiles human aortic endothelial cells in vitro and atherosclerotic lesions ex vivo, revealing heterogeneous subtypes and their responses to perturbations.

The paper uses single-cell time-resolved multi-omics to reveal apoptotic and ferroptotic heterogeneity in macrophage-derived foam cells during atherosclerosis progression.

The paper uses proteogenomic integration to identify CXCL10 as a mediator of IL-6 signaling effects on atherosclerosis, showing its association with cardiovascular disease risk and lesion characteristics.

This study identifies PDGFD as a CAD risk gene, showing it promotes SMC expansion, migration, and inflammation, contributing to vascular calcification and plaque recruitment.

This study uses single-cell RNA sequencing to analyze aortic cellular composition and responses in mice under high-fat diet and MSC_ITGB3 treatment, revealing changes in cell types and signaling pathways.

The paper links LIPA risk alleles to increased monocyte/macrophage LIPA expression, which exacerbates atherosclerosis through enhanced PU.1 binding and altered macrophage function.

This study shows that targeting scavenger receptors Stabilin-1 and Stabilin-2 reduces atherosclerosis by altering the plasma proteome, which suppresses monocyte/macrophage activity.

The paper shows that loss of PRMT2 in myeloid cells impairs atherosclerosis regression in normoglycemic mice, mimicking diabetic conditions, through increased inflammation and macrophage dysfunction.

This paper develops a mouse model to study how bacterial pneumonia affects atherosclerosis progression in ApoE-deficient mice through systemic inflammation.

This study shows that SAMD1 ablation in mice leads to embryonic lethality and failure of angiogenesis, suggesting a critical role in vascular development.

This study shows that MK2 inhibitors TBX-1 and TBX-2 improve glucose metabolism and reduce atherosclerotic plaque instability in mice with established atherosclerosis.

This study shows that inhibiting LXRα phosphorylation in hematopoietic cells reduces inflammation and improves atherosclerosis and obesity by altering macrophage and adipose tissue gene expression.

This study identifies SVEP1 as a novel coronary artery disease locus that promotes atherosclerosis by affecting vascular smooth muscle cell function and signaling pathways.