Atherosclerosis and Cardiovascular Diseases

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

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.

This study uses single-cell RNA sequencing to identify metabolic changes and gene signatures in atherosclerosis progression, revealing altered metabolic pathways and cell-cell interactions.

This study shows Epsins regulate smooth muscle cell reprogramming by modulating OCT4 and KLF4, with implications for coronary artery disease.

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

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.

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 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 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.

The paper identifies a genetic variant associated with increased carotid plaque vulnerability but not with cardiovascular disease risk in humans.

The paper analyzes single-cell transcriptomes of atherosclerotic plaques and adjacent tissue to identify gene drivers of cellular transdifferentiation and inflammatory processes.

The paper identifies TH17-related gene expression patterns in unstable angina patients, suggesting a link between TH17 inflammation and atherosclerosis.