Arteriosclerosis, Thrombosis, and Vascular Biology最新文献

{"title":"Hemodynamic Environments for the Progression of Carotid Stenosis: The NHO Carotid CFD Study.","authors":"Shunichi Fukuda, Yuji Shimogonya, Aoi Watanabe, Yuko Yoshimoto, Setsurou Maruyama, Naohiro Yonemoto, Kazuha Fujiwara, Miyuki Fukuda, Akihiro Yasoda","doi":"10.1161/ATVBAHA.125.322928","DOIUrl":"10.1161/ATVBAHA.125.322928","url":null,"abstract":"<p><strong>Background: </strong>Hemodynamic stress plays an important role in the development of atherosclerosis. It is difficult to sufficiently predict the progression of atherosclerosis and consequent stenosis based on known risk factors alone. This may be partly because the hemodynamic environments that promote stenosis progression remain unclear. The carotid bifurcation is the preferred site of atherosclerosis. In this prospective observational study, we sought to identify hemodynamic predictors of carotid stenosis progression.</p><p><strong>Methods: </strong>Computational fluid dynamics analysis was performed using arterial geometry and flow velocity specific to individual patients. Hemodynamic metrics were compared by multivariate analysis between the presence or absence of stenosis progression, using known risk factors as confounding factors.</p><p><strong>Results: </strong>A total of 545 patients were enrolled, and 361 stenotic arteries in 313 patients were analyzed, 38 of which had progressive stenosis. Among the carotid arteries with 30% to 55% area stenosis, those with stenosis progression had significantly lower time-averaged wall shear stress (WSS; odds ratio [OR], 0.078 [95% CI, 0.012-0.492]; <i>P</i>=0.0067) distal to the stenosis site and significantly higher oscillatory shear index (OR, 2.37 [95% CI, 1.17-4.82]; <i>P</i>=0.016). Among carotid arteries with 56% to 70% stenosis, those with stenosis progression had significantly higher time-averaged WSS (OR, 2.36 [95% CI, 1.19-4.72]; <i>P</i>=0.014) and transverse WSS (OR, 3.03 [95% CI, 1.45-6.34]; <i>P</i>=0.0033), a metric for multidirectional WSS disturbance, at the stenotic site and significantly higher transverse WSS (OR, 2.30 [95% CI, 1.20-4.42]; <i>P</i>=0.012) at the distal site. Arteries with 71% to 99% stenosis and stenosis progression had significantly higher oscillatory shear index (OR, 1.91 [95% CI, 1.05-3.47]; <i>P</i>=0.033) at the distal site.</p><p><strong>Conclusions: </strong>These data suggest the specific hemodynamic environments involved in the stenosis progression at bifurcation and that hemodynamic risk for stenosis progression differs depending on the degree of stenosis. Combining these hemodynamic predictors with known risk factors may allow a more accurate selection of cases at high risk of progression.</p>","PeriodicalId":8401,"journal":{"name":"Arteriosclerosis, Thrombosis, and Vascular Biology","volume":" ","pages":"1448-1458"},"PeriodicalIF":7.4,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144274116","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"LncRNA-536 and RNA-Binding Protein RBM25 Interactions in Pulmonary Artery Smooth Muscle Cells: Implications in Pulmonary Hypertension.","authors":"Aatish Mahajan, Sivasankar Chandran, Ashok Kumar, Ling Chen, Navneet K Dhillon","doi":"10.1161/ATVBAHA.125.322734","DOIUrl":"10.1161/ATVBAHA.125.322734","url":null,"abstract":"<p><strong>Background: </strong>In this study, we define the mechanistic association between long noncoding RNA: ENST00000495536 (lnc-536) and transcription factor HOXB13 (homeobox B13) in mediating proproliferative smooth muscle phenotype associated with pulmonary hypertension.</p><p><strong>Methods: </strong>In vitro knockdown or knockin, along with RNA pull-down and immunoprecipitation studies, were used to evaluate the role of lnc-536 and HOXB13 in regulating pulmonary arterial smooth muscle cell (PASMCs) phenotype. The in vivo role was determined by injecting lnc-536 antisense oligos in pulmonary hypertensive rats.</p><p><strong>Results: </strong>Increased levels of lnc-536 promote the proliferative phenotype of PASMCs by downregulating the expression of the tumor suppressor: HOXB13. Knockdown of lnc-536 and overexpression of HOXB13 in proliferative PASMCs resulted in increased expression of VGLL4 (vestigial-like family member 4), a negative regulator of Hippo and Wnt (Wingless-related integration site) signaling pathways, with a corresponding decrease in TEAD4 (TEA domain family member 1) expression. The lnc-536 pull-down assay and RNA-immunoprecipitation demonstrated the interactions of lnc-536 with RBP (RNA-binding protein): RBM25 (RNA-binding motif 25) and direct interactions of RBM25 with SFPQ (splicing factor proline/glutamine-rich), a transcriptional regulator that has a binding motif on HOXB13. The knockdown of RBM25 in the hyperproliferative PASMCs resulted in increased interactions of SFPQ and HOXB13 mRNA while attenuating PASMC proliferation. Furthermore, the increased levels of lnc-536 and decreased levels of HOXB13 were observed in PASMCs from idiopathic pulmonary hypertension patients but not in cells from familial pulmonary hypertension patients. We confirmed that lnc-536 contributes to the RBM25-mediated remodeling of the SFPQ-HOXB13 complex in the idiopathic PAH-PASMCs as well. Finally, in vivo inhibition of lnc-536 using GapmeRs (Gapmer antisense oligonucleotides) in Sugen-hypoxia and HIV-transgenic pulmonary hypertension rats prevented the increase in right ventricular systolic pressure, right ventricular hypertrophy/fibrosis, and pulmonary vascular remodeling with a parallel increase in HOXB13 expression in rat PASMCs.</p><p><strong>Conclusions: </strong>Lnc-536 acts as a decoy for RBM25, which in turn sequesters SFPQ, leading to a decrease in HOXB13 expression and hyperproliferation of smooth muscle cells by potentially regulating Wnt and Hippo signaling associated with PAH development.</p>","PeriodicalId":8401,"journal":{"name":"Arteriosclerosis, Thrombosis, and Vascular Biology","volume":" ","pages":"e374-e391"},"PeriodicalIF":7.4,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12286719/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144493820","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Direct Interleukin-6 Inhibition Blunts Arterial Thrombosis by Reducing Collagen-Mediated Platelet Activation.","authors":"Stefano Ministrini, Luca Liberale, Yustina M Puspitasari, Jiaying Han, Kilian Kirmes, Leonhard Paul Unkelbach, Amedeo Tirandi, Rebecca Niederberger, Susan Bengs, Jürg H Beer, Fabrizio Montecucco, Peter Libby, Thomas F Lüscher, Dario Bongiovanni, Giovanni G Camici","doi":"10.1161/ATVBAHA.125.322533","DOIUrl":"10.1161/ATVBAHA.125.322533","url":null,"abstract":"<p><strong>Background: </strong>Recent clinical trials demonstrated a reduction in biomarkers of thrombosis and inflammation in patients with very high cardiovascular risk treated with the anti-IL-6 (interleukin 6) monoclonal antibody ziltivekimab. However, if and how direct IL-6 inhibition exerts antithrombotic effects remains unknown. This translational project aimed to investigate the effect of direct IL-6 inhibition on experimental arterial thrombus formation and its underlying cellular mechanisms.</p><p><strong>Methods: </strong>Three-month-old C57BL/6J male and female mice received very low dose lipopolysaccharide for 4 weeks; in addition to lipopolysaccharide, during the fourth week, mice were randomized to receive either anti-mouse IL-6 monoclonal antibody 200 μg or IgG1 isotype control. Thrombosis of the right common carotid artery was induced by endothelial-targeted laser injury. Coagulation factors and platelet reactivity were assessed in treated mice and controls. Platelets were isolated from whole blood and their reactivity to different chemical stimuli was measured by fluorescence-activated cell sorting. Additionally, whole blood samples from patients with a history of percutaneous coronary intervention were incubated ex vivo with either ziltivekimab biosimilar or IgG1 isotype control. Platelet reactivity at rest and in response to diverse chemical stimuli was quantified by fluorescence-activated cell sorting.</p><p><strong>Results: </strong>Mice with low-grade chronic inflammation treated with anti-IL-6 monoclonal antibody displayed significantly blunted thrombus formation, without any significant difference in coagulation factors. Ex vivo stimulation with Collagen-rP (collagen-related peptide) significantly activated platelets isolated from control mice but not those obtained from mice treated with anti-IL-6 monoclonal antibody. Similarly, platelet reactivity from patients with previous percutaneous coronary intervention fell significantly after ex vivo treatment with ziltivekimab biosimilar.</p><p><strong>Conclusions: </strong>Direct IL-6 inhibition blunts thrombus formation by reducing collagen-induced platelet activation. These findings offer a potential mechanistic explanation for the results observed in the RESCUE trial and support the rationale of the ongoing ZEUS trial (Ziltivekimab Cardiovascular Outcome Study).</p>","PeriodicalId":8401,"journal":{"name":"Arteriosclerosis, Thrombosis, and Vascular Biology","volume":" ","pages":"1432-1439"},"PeriodicalIF":7.4,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12278750/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144324367","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Remembering Dr Janet T. Powell.","authors":"Ann Marie Schmidt, Robert A Hegele","doi":"10.1161/ATVBAHA.125.323274","DOIUrl":"https://doi.org/10.1161/ATVBAHA.125.323274","url":null,"abstract":"","PeriodicalId":8401,"journal":{"name":"Arteriosclerosis, Thrombosis, and Vascular Biology","volume":"45 8","pages":"1343-1345"},"PeriodicalIF":7.4,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144697542","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Antisense Oligonucleotide Targeting Sortilin Reduces Vascular Calcification in Mice in a Sex-Dependent Manner.","authors":"Adrien Lupieri, Dakota Becker-Greene, Thanh-Dat Le, Marina M Roschel, Prabhash K Jha, Abhijeet R Sonawane, Adam Mullick, Sotirios Tsimikas, Shiori Kuraoka, Sasha A Singh, Masanori Aikawa, Elena Aikawa","doi":"10.1161/ATVBAHA.124.321999","DOIUrl":"10.1161/ATVBAHA.124.321999","url":null,"abstract":"<p><strong>Background: </strong>Atherosclerotic calcification is a complex pathological process associated with an increased risk of cardiovascular events. Despite extensive research, this disorder has no effective therapeutic strategies. In this study, we evaluated the therapeutic potential of silencing Sort (sortilin) expression in vivo using antisense oligonucleotide (ASO-Sort1) to reduce the development of atherosclerosis and associated calcification.</p><p><strong>Methods: </strong>Male and female <i>Ldlr</i>^-/- (low-density lipoprotein receptor knock-out) mice were fed a high-fat diet and treated with ASO-Sort1 for 15 weeks. After ASO-Sort1 treatment, we evaluated atherosclerotic lesion formation and calcification through molecular imaging and histological techniques. The levels of plasma lipid and inflammatory molecules were determined. Unbiased liquid chromatography-mass spectrometry-based proteomics of aortic arches was conducted to investigate the sex-specific regulation in ASO-Sort1-treated mice. To validate our in vivo findings, we conducted in vitro experiments to examine whether β-estradiol treatment of mouse smooth muscle cells promotes calcification independently of Sort.</p><p><strong>Results: </strong>ASO targeted primarily arterial smooth muscle cells, leading to a comparable reduction of aortic Sort1 expression by ≈57% in males and 52% in females. Although ASO-Sort1 did not affect the size of atherosclerotic lesions, it significantly reduced necrotic core development by 60% in male and 40% in female mice. In addition, it prevented aortic calcification by >50% only in male mice. Furthermore, proteome analysis revealed that while this treatment reduced vesicular trafficking, immune system, and extracellular matrix organization pathways in both male and female mice, it reduced autophagy-related processes specifically in males. In vitro results indicated that β-estradiol promotes calcification in smooth muscle cells treated with ASO-Sort1 by altering autophagy.</p><p><strong>Conclusions: </strong>Targeting Sort using antisense technology is effective in preventing vascular calcification in male mice. This unexpected outcome highlighted a novel sex-dependent discrepancy of the calcification pathway implicating the alteration of autophagy by β-estradiol and Sort.</p>","PeriodicalId":8401,"journal":{"name":"Arteriosclerosis, Thrombosis, and Vascular Biology","volume":" ","pages":"1398-1415"},"PeriodicalIF":7.4,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12503371/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144274115","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association Between the Amount of Carotid Perivascular Adipose Tissue and Prior Ischemic Stroke: An MR Imaging Study.","authors":"Shuwan Yu, Ran Huo, Xueyi Chen, Xiaowei Song, Huiyu Qiao, Zihan Ning, Huimin Xu, Dandan Yang, Decheng Meng, Ning Xu, Zixuan Lin, Ying Liu, Xihai Zhao","doi":"10.1161/ATVBAHA.125.322687","DOIUrl":"10.1161/ATVBAHA.125.322687","url":null,"abstract":"<p><strong>Background: </strong>This study aimed to explore the association between the amount of carotid artery perivascular adipose tissue (PVAT) quantified by magnetic resonance imaging and prior cerebral infarction.</p><p><strong>Methods: </strong>A total of 139 patients (mean age, 64.4±8.2 years; 112 men) with moderate-to-severe atherosclerotic stenosis referred to carotid endarterectomy were included and underwent multicontrast magnetic resonance vessel wall and brain imaging. The amount of carotid artery PVAT with vulnerable plaque components on magnetic resonance images of each patient was quantitatively analyzed, and the measurements included the average PVAT area, PVAT area index, and PVAT volume index. The amount measurements of PVAT at slices with vulnerable plaque between patients with and without prior cerebral infarction were compared. Logistic regression analyses were conducted to determine the association between the amount measurements of PVAT and prior cerebral infarction.</p><p><strong>Results: </strong>Patients with prior cerebral infarction showed significantly higher PVAT area, PVAT area index, and PVAT volume index compared with those without (all <i>P</i><0.01). The carotid PVAT area (odds ratio [OR], 1.015 [95% CI, 1.003-1.028]; <i>P</i>=0.018), PVAT area index (OR, 2.051 [95% CI, 1.084-3.880]; <i>P</i>=0.027), and PVAT volume index (OR, 2.864 [95% CI, 1.343-6.108]; <i>P</i>=0.006) on the index side were significantly associated with prior cerebral infarction in univariate logistic regression. After adjusting for clinical confounding factors and plaque features, the associations between carotid PVAT area (OR, 1.028 [95% CI, 1.008-1.048]; <i>P</i>=0.006), PVAT area index (OR, 3.587 [95% CI, 1.451-8.870]; <i>P</i>=0.006), and PVAT volume index (OR, 6.053 [95% CI, 2.048-17.889]; <i>P</i>=0.001) and prior cerebral infarction remained statistically significant.</p><p><strong>Conclusions: </strong>The amount of PVAT in carotid artery with vulnerable plaques is independently associated with prior cerebral infarction and may, therefore, be related to the occurrence of ischemic stroke.</p>","PeriodicalId":8401,"journal":{"name":"Arteriosclerosis, Thrombosis, and Vascular Biology","volume":" ","pages":"1440-1447"},"PeriodicalIF":7.4,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144224167","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Potential Roles of SNX17, Rab11, and Rab5 in LDLR Recycling.","authors":"Xiaofei Zhao, Shiyin Long, Meiqi Zhu, Hong Hao, Ying Liao, Caiping Zhang, Zhenguo Liu","doi":"10.1161/ATVBAHA.125.322498","DOIUrl":"10.1161/ATVBAHA.125.322498","url":null,"abstract":"<p><p>Atherosclerotic cardiovascular disease is a leading cause of morbidity and mortality globally. Elevated levels of serum LDL-C (low-density lipoprotein cholesterol) represent a significant risk factor for atherosclerosis. LDLR (low-density lipoprotein receptor) plays a critical role in LDL-C uptake and clearance, with its recycling to the cell surface being essential for maintaining LDLR availability. However, the molecular mechanisms underlying LDLR homeostasis and recycling remain poorly defined. SNX (sorting nexin) proteins and Rab (Ras-associated binding protein) GTPases are key regulators of vesicle transport and endosomal sorting and are implicated in LDLR endocytosis, recycling, and subsequent cholesterol metabolism. This review aims to summarize the data on the roles of SNX17, Rab11, and Rab5 in LDLR recycling and endosomal dynamics, highlighting their potential as therapeutic targets for managing dyslipidemia and associated diseases.</p>","PeriodicalId":8401,"journal":{"name":"Arteriosclerosis, Thrombosis, and Vascular Biology","volume":" ","pages":"e338-e354"},"PeriodicalIF":7.4,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144324370","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hepatic Inactivation of Carnitine Palmitoyltransferase 1a Lowers ApoB-Containing Lipoproteins in Mice.","authors":"Robert N Helsley, Mikala M Zelows, Victoria P Noffsinger, Garrett B Anspach, Nikitha Dharanipragada, Anna E Mead, Isidoro Cobo, Abigail Carter, Qinglin Wu, Irina Shalaurova, Kai Saito, Josh M Morganti, Scott M Gordon, Gregory A Graf","doi":"10.1161/ATVBAHA.125.322473","DOIUrl":"10.1161/ATVBAHA.125.322473","url":null,"abstract":"<p><strong>Background: </strong>Genome- and epigenome-wide association studies have associated variants and methylation status of CPT1a (carnitine palmitoyltransferase 1a) to reductions in VLDL (very low-density lipoprotein) cholesterol and triglyceride levels. The objective of this study was to determine the mechanisms by which CPT1a-dependent mitochondrial fatty acid oxidation influences hepatic and lipoprotein metabolism.</p><p><strong>Methods: </strong>Eight-week-old male and female <i>Cpt1a</i>-floxed mice (<i>Cpt1a</i>^fl/fl) and <i>Cpt1a</i>-floxed mice expressing the human apo B₁₀₀ transgene (<i>Cpt1a</i>^fl/fl/B100^Tg) were administered control adeno-associated virus or adeno-associated virus encoding Cre-recombinase under control of a liver-specific promoter (TBG-Cre [thyroxin-binding globulin]). Control and liver-specific knockout mice were placed on a low-fat control or western-type diet (42% kcal fat, 0.2% cholesterol) for 16 weeks. Livers were collected and used for histological and lipid analysis, while gene and protein expression were measured by bulk RNA-sequencing and immunoblotting, respectively. Lipoprotein composition in plasma was determined by size exclusion chromatography and nuclear magnetic resonance. Rates of VLDL-triglyceride secretion were quantified after lipase inhibition with poloxamer 407. Liquid and gas chromatography-mass spectrometry were used to measure bile acid species and fecal neutral sterols, respectively.</p><p><strong>Results: </strong>We report significant associations between the presence of <i>CPT1a</i> SNPs (single nucleotide polymorphisms) and reductions in plasma cholesterol, as well as positive associations between hepatic Cpt1a expression and plasma cholesterol levels across inbred mouse strains. Mechanistic studies show that both wild-type and human apo B₁₀₀ (apoB)-transgenic mice with liver-specific deletion of <i>Cpt1a</i> (liver-specific knockout) display lower circulating apoB levels consistent with reduced LDL (low-density lipoprotein)-cholesterol and LDL particle number. Despite a reduction in steady-state plasma lipids, VLDL-triglyceride and VLDL cholesterol secretion rates are increased, suggesting accelerated clearance of apoB-LPs (apoB-containing lipoproteins) in liver-specific knockout mice. Mechanistic approaches show greater PPARα (peroxisome proliferator-activated receptor α) signaling which favors enhanced lipoprotein lipase-mediated metabolism of apoB-LPs, including increases in apo AIV and apo CII and reductions in apo CIII and Angptl3 (angiopoietin-like 3).</p><p><strong>Conclusions: </strong>These studies provide mechanistic insight linking genetic variants and methylation status of <i>CPT1a</i> to reductions in circulating apoB-LPs in humans.</p>","PeriodicalId":8401,"journal":{"name":"Arteriosclerosis, Thrombosis, and Vascular Biology","volume":" ","pages":"1368-1388"},"PeriodicalIF":7.4,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12286734/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144274117","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Change in Arterial Stiffness Is Associated With Change in Blood Glucose: Longitudinal Study in the Whitehall II Cohort.","authors":"Rachel E Climie, S Rehman, E J Brunner, P Boutouyrie, R M Bruno, J P Empana","doi":"10.1161/ATVBAHA.124.322001","DOIUrl":"10.1161/ATVBAHA.124.322001","url":null,"abstract":"<p><strong>Background: </strong>Type 2 diabetes is associated with elevated large artery stiffening, but arterial stiffening may also precede the development of type 2 diabetes. Whether the change in arterial stiffness over time is associated with dysglycemia across the entire spectrum of blood glucose concentration is unknown. Therefore, the primary objective of this study was to quantify the association between the change in arterial stiffness (exposure) and glycemic concentration (outcome).</p><p><strong>Methods: </strong>Within the prospective WHS II (Whitehall II Study), arterial stiffness was first measured in the 2007/09 examination round (baseline for the current study) and again in 2012/13, using the noninvasive, gold-standard method of carotid to femoral pulse wave velocity (cfPWV). Change in cfPWV was determined as cfPWV in 2012/13-cfPWV-cfPWV in 2007/09. Fasting blood glucose concentrations were measured at baseline (2007/09) and follow-up in 2012/13 and 2015/16.</p><p><strong>Results: </strong>There were 2632 participants without prior type 2 diabetes and cfPWV measured at 2 timepoints with follow-up in 2012/13 and 2282 with follow-up in 2015/16. Greater change in cfPWV was associated with significantly higher fasting glucose concentration at follow-up in 2012/13 and 2015/16 independently of confounders including cfPWV and fasting glucose levels at baseline (<i>P</i><0.001 for both). Greater change in cfPWV was significantly and independently associated with a greater change in fasting glucose concentration over the same period (2007/09-2012/13) and beyond (2007/09-2015/16).</p><p><strong>Conclusions: </strong>Minimizing premature arterial stiffening over time could be a valuable strategy for the prevention of glucose dysregulation and overt type 2 diabetes.</p>","PeriodicalId":8401,"journal":{"name":"Arteriosclerosis, Thrombosis, and Vascular Biology","volume":" ","pages":"1459-1467"},"PeriodicalIF":7.4,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144324366","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"IL1β Secretion by Epididymal White Adipose Tissue Macrophages Regulates Myelopoiesis and Plaque Inflammation in Obese Mice and in Caloric Restriction.","authors":"Zhixing Li, Franziska Krautter, Maxwell La Forest, Edward A Fisher","doi":"10.1161/ATVBAHA.125.322789","DOIUrl":"10.1161/ATVBAHA.125.322789","url":null,"abstract":"","PeriodicalId":8401,"journal":{"name":"Arteriosclerosis, Thrombosis, and Vascular Biology","volume":" ","pages":"1468-1470"},"PeriodicalIF":7.4,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12286714/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144493819","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}