Atherosclerosis and Cardiovascular Diseases

This study evaluates the impact of biological sex on atherosclerosis in Apoe-/- and Ldlr-/- mice, finding sex-dependent differences in plaque burden and metabolic parameters.

This study shows that ARF6 promotes VSMC phenotypic switching and inflammatory signaling in atherosclerosis by modulating lipid uptake, cytokine production, and inflammatory pathways.

This study shows that high cholesterol induces epigenetic changes in hematopoietic stem cells that persist after cholesterol reduction, leading to systemic immunometabolic dysfunction.

The paper identifies p210-specific CD8+ T cells in human carotid atherosclerotic plaques from HLA-A02:01+ patients, linking their presence to plaque stability and suggesting immunotherapy potential.

This study shows chronic e-cigarette exposure accelerates atherosclerosis by reprogramming smooth muscle cells toward a chondrogenic phenotype through GRIN2A-dependent NMDAR signaling.

This study shows that Xcr1+ cDC1 cells promote atherosclerosis progression, as their depletion reduces plaque formation and T cell activation in mice.

This study shows that epsin deletion reduces foam cell formation and rewires vascular smooth muscle cell and endothelial functions in atherosclerosis.

This study identifies CD27+ γδ T cells as key drivers of atherosclerotic plaque instability and shows that targeting CXCR3 with AMG487 improves plaque stability.

This study identifies CCBE1 as a gene associated with mitochondrial dysfunction in atherosclerosis using transcriptomic analysis of endothelial cells from CAD patients.

This study identifies a novel pathway by which LDL triggers pro-fibrotic protein secretion in endothelial cells via Scarf1 and SNARE proteins.

This study shows TMAO affects cell type-specific pathways in mouse aorta, promoting atherosclerotic plaque instability by increasing apoptosis and reducing ECM formation.

The paper identifies CD8 T cells in HIV-positive individuals that promote endothelial inflammation via granzyme-dependent PAR1 activation, linking immune activation to cardiovascular risk.

This study identifies CCR2+ neutrophils in atherosclerotic plaques that promote instability through ROS production and NET release, and shows that targeting CCR2 reduces plaque destabilization.

This study shows that genetic silencing of KCa3.1 reduces atherosclerosis in ApoE null mice by decreasing lesion size and macrophage content.

This study identifies PKCε as a novel atheroprotective gene by showing its role in restricting lipid uptake in myeloid cells and reducing plaque vulnerability.

This study examines immune checkpoint expression in PAD patients and finds sex-specific changes in soluble PD-L2 and TIM-3 levels, along with increased PD-L2+ monocytes and TIM-3+ CD4+ T cells.

This study shows that GATA2 upregulation in macrophages promotes atherogenesis by inducing a stem cell-like transcriptional program that impairs cholesterol efflux and phagocytosis.

The paper identifies self-reactive B cells in atherosclerosis-associated tertiary lymphoid organs that produce high-affinity autoantibodies contributing to disease progression.

This study shows that neutrophil TLR2 signaling promotes lipid uptake and storage, contributing to atherosclerotic plaque growth.

This study shows that ApoE deficiency, not atherosclerosis, alters non-invariant NKT cell numbers and activation, highlighting the need to use ApoE-null mice cautiously in NKT cell research.

This study shows that CCR4 deficiency in mice worsens early atherosclerosis by impairing Treg function and promoting proinflammatory Th1 responses.

This study identifies ox-LDL-induced non-inflammatory changes in endothelial cells that are enriched for coronary artery disease risk.

This study shows that MyD88 promotes smooth muscle cell phenotypic modulation and fibrous cap formation in atherosclerosis by reducing cap SMC recruitment and preserving contractile phenotype.

This study shows LPHN2 is essential for flow-induced Notch activation to suppress inflammation and atherosclerosis in endothelial cells.

The paper identifies a VSMC transition linked to fibrous cap formation in atherosclerosis and shows PAR1 as a potential therapeutic target.

This study shows that loss of LATS1/2 in endothelial cells promotes a senescence-associated stemness (SAS) state, leading to atherothrombotic plaque formation through metabolic and mitochondrial dysregulation.

This study identifies STAT1-dependent genes in IFNγ-treated macrophages and links them to atherosclerosis through multi-omics analysis in human and mouse models.

This study identifies FAK activity as a mediator of disturbed flow-induced atherosclerosis through the VEGFR2-Cbl-NF-κB signaling pathway in endothelial cells.

The paper identifies a novel CD26+ fibroblast subpopulation in atherosclerosis using CITE-seq and shows its expansion into fibrous caps during disease progression.