Atherosclerosis and Cardiovascular Diseases

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 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 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.

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 shows that an anti-isoDGR antibody reduces atherosclerosis and metabolic dysfunction in ApoE-/- mice fed a Western diet.

This study classifies porcine atherosclerotic plaques into four types that correspond to human coronary atherosclerosis types, using morphological and cellular features from FH pigs fed a high-fat diet.

This study shows that IL-18 inhibition increases atherosclerosis lesions and necrotic cores in Jak2V617F clonal hematopoiesis mice, despite improving fibrous cap thickness.

The paper identifies macrophage-like vascular smooth muscle cells as dominant in early atherosclerosis and shows that targeting iron regulation inhibits their transition.

This study shows IL-17A promotes plaque instability in psoriatic atherosclerosis by enhancing macrophage inflammation and disrupting lipid metabolism.

This study shows that inhibiting endothelial AGO1 reduces vascular inflammation and atherosclerosis by blocking its non-canonical nuclear role in promoting NF-κB-driven inflammation.

The paper identifies female-biased VSMC gene regulatory networks and highlights MYH9 as a key regulator of fibrous plaque phenotype in females.

This study develops a metabolic syndrome mouse model by combining hypertension, dyslipidemia, and diabetes in apolipoprotein E knockout mice, showing increased atherosclerosis severity.

This study validates the two-hit hypothesis showing disturbed flow and hypercholesterolemia together reprogram endothelial cells to immune-like and foam cells during atherogenesis.

This study uses spatial transcriptomics to analyze immune cell organization in human coronary arteries across atherosclerosis stages, identifying relevant pathways and molecules for therapeutic targets.

This study shows that chronic inhaled benzene exposure worsens atherosclerosis in LDLR-KO mice by increasing T-cell proliferation and Th17 polarization, along with vascular smooth muscle cell changes.

This study identifies PRC2 as a driver of atherosclerosis by suppressing Klf2/4, and shows that inhibiting PRC2 with tazemetostat reduces plaque progression and improves stability.

This study identifies SMAD/FOXO1 complexes that mediate EndoMT in response to atheroprone flow, showing their role in atherosclerosis and suggesting targeting this interaction could reduce disease progression.

This study shows that deleting zyxin in endothelial cells reduces inflammation and atherosclerosis by affecting the zyxin-14-3-3β-YAP signaling pathway.

This study shows that latexin promotes neointimal formation by enhancing smooth muscle cell proliferation and macrophage migration in mice.

This study shows that subendothelial calcification increases arterial surface roughness and promotes LDL uptake, contributing to atherosclerosis.

This study shows dioxin exposure accelerates atherosclerosis by promoting inflammatory smooth muscle cell phenotypes and oxidative stress, with AHR in SMC providing protective effects.

This study shows that deleting CD45 in endothelial cells reduces atherosclerosis by inhibiting EndoMT and TGFβ signaling through increased FGFR2 and KLF2 expression.

This study shows cholesterol accumulation in macrophages impairs AKT signaling and HIF-1α-dependent glycolysis, but these effects are not synergistic in suppressing inflammation.

This study identifies sex-specific roles of inflammation and lipid-handling dysfunction in atherosclerosis using transcriptomic data from 391 human blood samples.

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