ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY动脉硬化、血栓形成与血管生物学
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY(英文缩写 ARTERIOSCL THROM VAS),ISSN 1079-5642,eISSN 1524-4636,中文译名:动脉硬化、血栓形成与血管生物学 是一本学术期刊。本页汇总该期刊的最新影响因子、分区信息以及最新收录于 PubMed 的文献,帮助您快速了解期刊全貌。
发文量统计区间：2025-09-28 至 2026-09-28，按本站收录文献的发表日期统计。
期刊介绍
历年影响因子趋势
| JCR 数据年份 | 影响因子 | JCR 分区 |
|---|---|---|
| 2021 | 10.514 | Q1 |
| 2022 | 8.700 | Q1 |
| 2023 | 7.400 | Q1 |
| 2024 | 7.400 | Q1 |
| 2025 | 8.800 | Q1 |
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY 最新收录文献
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2. {"_":" Promotes Endothelial Phenotypic Transition and Unstable Plaque Phenotype During Atherosclerosis.","i":["Twist1"]}
PMID:日期:2026-10-01Comprehensive investigation of endothelial cell (EC) dysfunction during atherosclerosis with single-cell omics has resulted in the proposal that ECs undergo multiple alternative cell fate decisions during disease, but lack of lineage tracing or spatial localization complicates interpretation of these data. , a causal gene for multiple atherosclerotic vascular diseases, is activated with low shear stress in ECs, and EC- knockout results in reduced atherosclerosis. However, it remains unclear how affects EC phenotype and plaque biology. We performed EC lineage tracing, in situ analysis, and scRNA-Seq (single-cell RNA-sequencing) in mice, both before disease and after 16 weeks of high-fat diet. We also performed these studies with 2 mouse models of EC deletion. We overexpressed in human coronary artery ECs exposed to different flow conditions, followed by bulk RNA-seq. Human scRNA-Seq data were used to validate key findings in the mouse model. We found that EC phenotypic modulation during atherosclerosis is characterized by both proinflammatory and endothelial-to-mesenchymal transition gene programs, occurring simultaneously along a single-cell fate transition. Human scRNA-Seq data validated a similar endothelial-to-mesenchymal transition during disease. We found that the commonly used conditional allele is hypomorphic, leading to reduced expression in multiple cell types. Using a mouse model of EC-specific deletion, we found reduced EC phenotypic modulation, decreased lesion size, and a more stable lesion phenotype. Integration of overexpression in human coronary artery ECs with the mouse scRNA-seq data identified specific -induced targets including CXCL12 and E-selectin during EC phenotypic modulation. Our study revealed important aspects of EC phenotypic modulation during atherosclerosis, unifying disparate observations in the field. We identified key cellular and molecular mechanisms underlying a top risk locus for multiple vascular diseases, highlighting the promotion of inflammatory endothelial-to-mesenchymal transition by as a key driver of disease risk.
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3. Disarming FcγRIIA: Separating Immunothrombosis From Protective Immunity.
PMID:日期:2026-10-01该文献暂无摘要。
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4. MAP17 Orchestrates SGLT2-Dependent Glycolytic Reprogramming to Drive Trained Immunity and Accelerate Atherosclerosis.
PMID:日期:2026-10-01Atherosclerosis is driven by metabolic-immune crosstalk, in which trained immunity sustains vascular inflammation. MAP17 (membrane-associated protein 17), a redox- and metabolism-regulating adaptor protein, functions as a potential upstream driver of SGLT2 (sodium-glucose cotransporter 2). We aimed to determine whether MAP17 links hyperglycemia to glycolytic activation, inflammatory polarization, and plaque progression in atherosclerosis. MAP17 expression and its correlations with clinical risk factors were analyzed in serum from 30 patients with atherosclerosis. A trained immunity model was established in bone marrow-derived macrophages via sustained high glucose and IFN-γ (interferon-γ)/lipopolysaccharide stimulation. Functional assays were performed after MAP17 overexpression/knockdown, SGLT2 silencing, or glycolysis inhibition. MAP17 was significantly coupregulated in patients with atherosclerosis, with the highest levels observed in those with concomitant diabetes or metabolic syndrome, and closely associated with elevated proinflammatory M1-like cytokines. Immunohistochemistry of carotid plaques confirmed its colocalization with SGLT2 within CD68 macrophage-rich, lipid-laden, and inflamed regions. In bone marrow-derived macrophages, high glucose robustly induced MAP17 expression, which unidirectionally upregulated SGLT2, enhanced glycolytic flux, increased lactate production, and promoted M1-like polarization and foam cell formation. MAP17 knockdown markedly suppressed SGLT2 expression, glycolysis, and TNF-α (tumor necrosis factor-α)/IL (interleukin)-1β secretion, whereas MAP17 overexpression restored glycolytic activity, proinflammatory phenotype, and foam cell generation even in SGLT2-deficient cells. In diabetic chimeric mice, MAP17 activation correlated with increased glycolytic marker expression, higher proinflammatory M1-like macrophage ratios, aggravated vascular inflammation, and greater plaque burden; these effects were mitigated by MAP17 or SGLT2 silencing, or by glycolysis inhibition. MAP17 is a key upstream controller of the SGLT2-glycolysis axis that promotes trained immunity and accelerates atherosclerosis. Targeting MAP17 may disrupt the metabolic-inflammatory feedback loop and represents a promising therapeutic strategy for diabetic atherosclerosis.
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6. Metabolites Associated With Long-Term Risk of Peripheral Artery Disease: The ARIC Study.
PMID:日期:2026-10-01Lower extremity peripheral artery disease (PAD) is a major contributor to cardiovascular morbidity and mortality; however, the metabolic pathways underlying disease development and progression are poorly understood. We conducted a prospective cohort study of 3759 participants from the ARIC study (Atherosclerosis Risk in Communities; mean age, 53.5 years; 60% women; 62% Black participants) with untargeted metabolomic profiling at baseline (1987-1989). Incident PAD (458 cases) and its severe form with rest pain or tissue loss, critical limb ischemia (CLI; 135 cases), were identified through hospitalization codes over a median follow-up of 27 years. We used Cox regression with adjustment for traditional risk factors and accounted for multiple testing using a false discovery rate correction at a threshold of 0.05. Risk prediction improvement was evaluated using Harrell C statistics and the net reclassification improvement. Thirteen metabolites were significantly associated with incident PAD and primarily reflected dysregulated glycemic control, impaired redox balance, and altered lipid remodeling (eg, higher levels of mannose and lower levels of 1,5-anhydroglucitol, gamma-glutamyl dipeptides, and lysophospholipids). For CLI, 18 metabolites were identified, 11 of which were unique to CLI and reflected intensified oxidative and bioenergetic stress (eg, homocitrulline, arabonate, and 1-linoleoylglycerol). Metabolites significantly improved risk prediction for PAD beyond traditional risk factors (∆C statistic, 0.017 [95% CI, 0.008-0.025] from a base C statistic of 0.770; net reclassification improvement, 0.053 [95% CI, 0.018-0.083]) and particularly CLI (∆C statistic, 0.041 [95% CI, 0.018-0.064] from a base C statistic of 0.823; net reclassification improvement, 0.176 [95% CI, 0.085-0.268]). Distinct metabolomic profiles were associated with incident PAD and CLI years before clinical onset, highlighting dysregulated glycemic control, impaired redox balance, and altered lipid remodeling as key underlying pathways. These findings suggest that circulating metabolites may serve as early indicators of metabolic health relevant to PAD risk identification and progression to advanced disease.
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7. Na/K-ATPase Signaling in Adipocytes Promotes Atherosclerosis.
PMID:日期:2026-10-01Adipocyte dysfunction is closely associated with oxidative stress and chronic inflammation, which contribute to systemic metabolic disturbances and atherosclerosis. We previously identified the NKA (Na/K-ATPase) α1 subunit as a signal transducer that activates Src-family kinases and promotes oxidative stress and inflammation in various cell types, including adipocytes and macrophages. NaKtide, a peptide inhibitor of NKA signaling, has been shown to reduce systemic oxidative stress and inflammation in vivo. In this study, we investigated the role of adipocyte-specific NKA signaling in atherosclerosis. Adipocyte-specific NaKtide was delivered to mice using a lentiviral vector under the adiponectin promoter. The mice were then fed a Western diet for 12 weeks to induce atherosclerosis and then assessed for atherosclerotic plaque burden in the aortic arch and at the level of the aortic sinus. Inflammatory and oxidative stress markers were analyzed in adipose tissue and plasma. Adipocyte-specific NaKtide reduced atherosclerotic plaque area by 67% in the aortic arch and by 48% in the aortic sinus. CD68+ (cluster of differentiation 68) macrophage content and α-SMA+ (α-smooth muscle actin) smooth muscle cell content in the aortic sinus were decreased by 45% and 53%, respectively. These vascular improvements were accompanied by dampened adipose tissue inflammation and oxidative stress, improved glucose tolerance, and reduced systemic inflammation. These findings highlight a critical contributing role for adipocyte NKA signaling in atherosclerosis, suggesting an important endocrine and paracrine influence of adipose tissue on large artery atherogenesis and supporting the therapeutic potential of targeting NKA in cardiometabolic disease.
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8. Relaxin-3/RXFP1 Axis Regulates the Phenotypic Switch of Diabetic Vascular Smooth Muscle Cells by Inhibiting H3K18la-Mediated Egfr Transcription.
PMID:日期:2026-10-01The phenotypic switching of vascular smooth muscle cells (VSMCs) is a critical pathophysiological mechanism of diabetic vascular remodeling. There is increasing evidence indicating that endogenous relaxin-3 exhibits cardiovascular effects, including vasodilation, reversal of ventricular remodeling, and attenuation of myocardial fibrosis. This study investigates the role of relaxin-3 as a key regulator in the phenotypic switching of VSMCs and elucidates its underlying mechanisms. We generated a diabetic rat model to investigate the biological roles of relaxin-3 in diabetic vascular remodeling. Metabolomic profiling characterized relaxin-3-induced metabolic changes in VSMCs under high glucose treatment. Combined chromatin immunoprecipitation sequencing and RNA sequencing data were used to further investigate the gene regulatory mechanisms of relaxin-3 in the phenotypic switching of VSMCs and target genes regulated by H3K18la (histone H3 lysine 18 lactylation). Relaxin-3 and its receptor RXFP1 (relaxin family peptide receptor 1) were upregulated in diabetic human and rat aortas. Silencing of relaxin-3 or RXFP1 expression inhibited VSMC contractile phenotype protein expression and promoted VSMC proliferation. Relaxin-3 treatment mitigated the phenotypic switching of VSMCs via RXFP1, preserving VSMCs' contractile phenotype. Further, relaxin-3 treatment lowered the glycolytic rate and lactate production during the phenotypic switching of VSMCs and decreased histone lactylation. Mechanistically, relaxin-3 suppressed LDHA (lactate dehydrogenase A)-mediated lactate production and H3K18la-mediated (epidermal growth factor receptor) transcription, and blocked PKM2 (pyruvate kinase M2) nuclear translocation, thereby preventing PKM2/β-catenin complex formation. Relaxin-3 alleviated the phenotypic switching of diabetic VSMCs through a dual mechanism: inhibiting lactate-mediated H3K18la and disrupting the intranuclear PKM2/β-catenin interaction, thereby preserving the contractile VSMC phenotype.
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9. SEPTIN7 Deficiency Disrupts Endothelial Integrity and Causes Myxomatous Valve Disease in Juvenile Mice.
9. SEPTIN7缺乏会破坏幼年小鼠的内皮完整性并导致粘液瘤性瓣膜病PMID:日期:2026-10-01Myxomatous valve degeneration is a major contributor to adult-onset valvular disease, with congenital valve abnormalities being a predisposing factor. However, the molecular networks that govern heart valve development, particularly postnatal valve maturation, remain poorly understood. This study was designed to investigate the role of GTP‑binding SEPTIN proteins in heart valve formation. We generated endocardial lineage-specific conditional knockout mouse models targeting , , or . Cardiac phenotypes were assessed using histopathology, immunohistochemistry, and molecular analyses. Mice lacking or developed normally without detectable abnormalities. In contrast, mutant mice exhibited juvenile lethality due to congestive heart failure caused by severe aortic stenosis. Although valve structure appeared normal at birth, mutants progressively developed myxomatous degeneration, characterized by leaflet thickening, extracellular matrix disorganization, and inflammatory infiltration. Loss of disrupted valvular endothelial integrity, with increased intercellular gaps and reduced expression of cell-cell junction proteins. Mechanistically, ablation inhibited endothelial cell proliferation, most likely through upregulation of the cell cycle inhibitor p21. Altogether, our findings identify a previously unrecognized role of SEPTIN7 in postnatal heart valve maturation and homeostasis, wherein it safeguards endothelial integrity. This discovery provides critical mechanistic insights into the pathogenesis of pediatric myxomatous valve disease.
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10. Time of Day as a Biological Variable in Cardiovascular and Kidney Disease Research: A Scientific Statement From the American Heart Association.
PMID:日期:2026-10-01Lifestyle behaviors such as diet, physical activity, and sleep play a prominent role at every stage of cardiometabolic disease. These behaviors follow daily, circadian rhythms in humans. These endogenous biological rhythms are controlled by an autonomous molecular clock present in every cell of the body. This presents a translational mismatch wherein in-clinic human procedures are typically performed on awake, active individuals in a fed state, whereas in-laboratory procedures on rodents are often conducted in the daytime during their inactive, rest phase, when they are minimally motivated to eat. This American Heart Association scientific statement is intended to raise awareness that time of day is a biological variable that must be considered as a key modulatory factor in all facets of biomedical research from basic to clinical science. The entirety of the cardiovascular and renal systems function in a circadian fashion, making the time of day critically important in understanding basic and clinical research. This daily variability ranges from gene expression to functional outputs and everything in between. Here, we provide rationale for why time of day needs to be considered in various aspects of experimental design and interpretation in research and provide what we believe are useful suggestions to strengthen the rigor and utility of cardiometabolic and kidney research.