Atherosclerosis and Cardiovascular Diseases

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.

The paper identifies gene signatures of endothelial-to-mesenchymal transition in human atherosclerotic tissue using combined in vitro and single-cell transcriptomic data.

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 shows that gut microbial metabolite imidazole propionate impairs endothelial function and promotes atherosclerosis in both human and animal models.

This study shows that the 9p21.3 CAD risk locus drives vascular smooth muscle cells to an osteochondrogenic state through ANRIL expression, leading to arterial calcification.

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 shows that free cholesterol accumulation in macrophages activates a PARP1 response to DNA damage, which suppresses lipopolysaccharide-induced inflammation through a non-enzymatic mechanism.

This study shows that overexpressing Fgf23 in male ApoE-/- mice increases atherosclerotic plaque burden and alters immune responses.

This study uses spatial transcriptomics to compare gene expression in intima and media of human coronary arteries, revealing dedifferentiated SMCs in DIT that differ from proinflammatory SMCs in atherosclerotic lesions.

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 shows that ASXL1 mutations in mice promote atherosclerosis by dysregulating innate immunity through impaired inhibition of NF-κB signaling.

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 shows that hypercholesterolemia causes coronary microvascular dysfunction in mice through enhanced lysosomal signaling in endothelial cells, which can be mitigated by ezetimibe.

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 the mitochondrial H2S donor AP39 reduces atherosclerosis by reprogramming macrophages and increasing UCP1 in vascular smooth muscle cells.

This study shows that the novel nested gene Aff3ir-ORF2 reduces atherosclerosis in mice by inhibiting IRF5-mediated inflammation under disturbed flow conditions.

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.