Arteriosclerosis, Thrombosis, and Vascular Biology最新文献

{"title":"NAD Metabolism Regulates Proliferation of Macrophages in Atherosclerosis.","authors":"Satyesh Sinha, Chantle R Swichkow, Lia Farahi, Miklós Péterfy, Calvin Pan, Zhiqiang Zhou, Marcus Seldin, Julia J Mack, Richard C Davis, Diana Shih, Aldons J Lusis","doi":"10.1161/ATVBAHA.125.323185","DOIUrl":"https://doi.org/10.1161/ATVBAHA.125.323185","url":null,"abstract":"<p><strong>Background: </strong>In genetic studies with the Hybrid Mouse Diversity Panel, we previously identified a chromosome 9 locus for atherosclerosis. We now identify NNMT (nicotinamide <i>N</i>-methyltransferase), an enzyme that degrades nicotinamide, as the causal gene in the locus and show that the underlying mechanism involves salvage of nicotinamide to nicotinamide adenine dinucleotide (NAD).</p><p><strong>Methods: </strong>Gain/loss of function studies in macrophages were performed to examine the role of NAD levels in macrophage proliferation and apoptosis in atherosclerosis.</p><p><strong>Results: </strong>Global inhibition of NNMT using an antisense oligonucleotide reduced atherosclerosis lesion area 5- to 10-fold in both male and female mice on a hyperlipidemic background. Selective inhibition of NNMT in liver and adipose, the major tissues expressing high levels of the enzyme, using siRNA, had little or no effect on atherosclerosis. Therefore, we hypothesized that levels of NAD in macrophages might contribute. This was confirmed by showing that transplantation with bone marrow from <i>Nnmt</i> knockout mice resulted in reduced lesional macrophage proliferation, increased macrophage apoptosis, and reduced atherosclerosis. Consistent with this conclusion, reduced expression of macrophage CD38, an enzyme that degrades NAD, reduced both macrophage proliferation and atherosclerosis. Moreover, cultured macrophages from heterozygous <i>Nnmt</i> knockout mice exhibited reduced proliferation, increased apoptosis, and an increased NAD/NADH ratio.</p><p><strong>Conclusions: </strong>These findings reveal a role for nicotinamide salvage and NAD turnover in macrophage proliferation and survival in the context of atherosclerosis.</p>","PeriodicalId":8401,"journal":{"name":"Arteriosclerosis, Thrombosis, and Vascular Biology","volume":" ","pages":""},"PeriodicalIF":7.4,"publicationDate":"2025-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145032631","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":"Single-Cell Analysis Reveals a Critical Role for Macrophage Epsins in Regulating the Origin of Foam Cells in Atherosclerosis.","authors":"Kulandaisamy Arulsamy, Kui Cui, Bo Zhu, Beibei Wang, Shahram Eisa-Beygi, Anna Voronova, Xinlei Gao, Krishan Gupta, Lili Zhang, Kaifu Chen, Hong Chen","doi":"10.1161/ATVBAHA.125.323288","DOIUrl":"https://doi.org/10.1161/ATVBAHA.125.323288","url":null,"abstract":"<p><strong>Background: </strong>Atherosclerosis is a chronic inflammatory disease characterized by the accumulation of lipid-laden foam cells and plaques within the arterial wall. Dysfunctional vascular smooth muscle cells (VSMCs), fibroblasts, endothelial cells, and macrophages contribute to disease progression. Here, we report that macrophage-specific expression of epsins, highly conserved endocytic adaptor proteins involved in clathrin-mediated endocytosis, accelerates atherosclerosis in Western diet-fed mice.</p><p><strong>Methods: </strong>WT/Apoe^-/- (Apoe-deficient) mice and littermates with a LysM-DKO/Apoe^-/- (myeloid-specific deletion of epsin 1/2 on an Apoe^-/- background) were generated and fed a Western diet for 16 weeks. Single-cell RNA sequencing was conducted to investigate the cellular and molecular mechanisms regulated by macrophage epsins during atherosclerosis. Findings from single-cell RNA sequencing were validated through metabolic profiling, qRT-PCR, immunostaining, and coculture experiments to assess associated phenotypic changes.</p><p><strong>Results: </strong>LysM-DKO/Apoe^-/- mice exhibited significantly reduced atherosclerotic foam cell formation compared with WT/Apoe^-/- controls. Single-cell RNA sequencing analysis identified 19 major cell types, including 6 VSMC and 5 macrophage subpopulations. Modulated VSMC1 and VSMC2 subtypes were associated with inflammation, migration, and VSMC-to-macrophage transition. These populations, along with foamy-Trem2 and inflammatory macrophages, were markedly reduced in LysM-DKO/Apoe^-/- mice. Transition of modulated VSMC2 subtype into macrophages was significantly inhibited, as confirmed by both computational analysis and experimental validation. In addition, macrophage epsin deletion reversed endothelial dysfunction, suppressed cholesterol- and glucose-mediated signaling, and reduced expression of proinflammatory ligands IL (interleukin)-1β and TNF-α (tumor necrosis factor α).</p><p><strong>Conclusions: </strong>Macrophage epsin deletion limits foam cell formation and preserves VSMC and endothelial cell phenotypes and functions. These findings reveal a potential therapeutic strategy targeting macrophage epsins to combat atherosclerosis.</p>","PeriodicalId":8401,"journal":{"name":"Arteriosclerosis, Thrombosis, and Vascular Biology","volume":" ","pages":""},"PeriodicalIF":7.4,"publicationDate":"2025-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145032646","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":"Estimated Glucose Disposal Rate and Risk of Stroke and Dementia in Nondiabetics: A UK Biobank Prospective Cohort Study.","authors":"Lei Liu, Yi Zheng, Kai Luo, Huihui Ma, Wei Jiang, Rong Luo, Caixia Pan, Tao He, Hongqiang Ren, Gary Tse, Tong Liu, Xiaoping Li","doi":"10.1161/ATVBAHA.125.322702","DOIUrl":"https://doi.org/10.1161/ATVBAHA.125.322702","url":null,"abstract":"<p><strong>Background: </strong>The estimated glucose disposal rate (eGDR) is a validated surrogate marker of insulin resistance. However, its association with stroke and dementia in nondiabetic populations remains insufficiently investigated.</p><p><strong>Methods: </strong>This prospective cohort study included nondiabetic participants from the UK Biobank. The outcomes in this study were stroke, ischemic stroke, hemorrhagic stroke, all-cause dementia, vascular dementia, and Alzheimer disease. Multivariable Cox regression and restricted cubic splines were used to examine the associations between eGDR and outcomes. Polygenic risk score analyses were applied to investigate interactions between eGDR and genetic risk.</p><p><strong>Results: </strong>Overall, 430 093 participants were included. During a follow-up of around 13.5 years, 10 307 stroke cases and 11 137 all-cause dementia cases were recorded. Restricted cubic splines analyses indicated nonlinear associations between eGDR and the risks of stroke and vascular dementia. Below specific thresholds (<7.64 for stroke, <7.60 for ischemic stroke, <7.75 for hemorrhagic stroke, and <8.31 for vascular dementia), eGDR levels were not significantly associated with these outcomes except a modest inverse association with overall stroke risk (hazard ratio [HR] 0.97 [95% CI, 0.95-0.99]; <i>P</i>=0.012). In contrast, above these thresholds, higher eGDR levels were associated with significantly reduced risks of stroke (HR, 0.80 [95% CI, 0.78-0.82]; <i>P</i><0.001), ischemic stroke (HR, 0.80 [95% CI, 0.78-0.81]; <i>P</i><0.001), hemorrhagic stroke (HR, 0.81 [95% CI, 0.78-0.84]; <i>P</i><0.001), and vascular dementia (HR, 0.89 [95% CI, 0.84-0.94]; <i>P</i><0.001). A linear inverse relationship was observed between eGDR and all-cause dementia and Alzheimer disease. The HR in the highest versus lowest quartile was 0.81 (95% CI, 0.75-0.88) for all-cause dementia and 0.73 (95% CI, 0.64-0.84) for Alzheimer disease. Stratified polygenic risk score analyses revealed a synergistic interaction between reduced eGDR and elevated genetic susceptibility.</p><p><strong>Conclusions: </strong>eGDR exhibited nonlinear associations with stroke and vascular dementia risk and linear inverse associations with all-cause dementia and Alzheimer disease in nondiabetic populations.</p>","PeriodicalId":8401,"journal":{"name":"Arteriosclerosis, Thrombosis, and Vascular Biology","volume":" ","pages":""},"PeriodicalIF":7.4,"publicationDate":"2025-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145032623","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":"ADP-Ribosylation in Experimental Atherosclerosis: A Potential Link Between Dyslipidemia and Inflammation in Cardiovascular Disease.","authors":"Diego V Santinelli-Pestana, Constance Delwarde, Taku Kasai, Shiori Kuraoka, Yuto Nakamura, Takeshi Okada, Julius L Decano, Sarvesh Chelvanambi, Rile Ge, Andrew K Mlynarchik, Katelyn Perez, Alesandra Campedelli, Abhijeet R Sonawane, Elena Aikawa, Sasha A Singh, Masanori Aikawa","doi":"10.1161/ATVBAHA.125.322497","DOIUrl":"10.1161/ATVBAHA.125.322497","url":null,"abstract":"","PeriodicalId":8401,"journal":{"name":"Arteriosclerosis, Thrombosis, and Vascular Biology","volume":" ","pages":""},"PeriodicalIF":7.4,"publicationDate":"2025-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144991543","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":"Platelet Activation and a Platelet Biosignature Are Associated With Cardiovascular Risk in Patients With Controlled Psoriasis.","authors":"Michael S Garshick, Kamelia Drenkova, Filipp Kazatsker, Isabelle Boothman, Matthew Muller, Florencia Schlamp, Elliot Luttrell-Williams, Kristen Lo Sicco, Andrea Neimann, Jose U Scher, Brittany Weber, Joel M Gelfand, James Krueger, Jill Buyon, Jeffrey S Berger","doi":"10.1161/ATVBAHA.125.322574","DOIUrl":"https://doi.org/10.1161/ATVBAHA.125.322574","url":null,"abstract":"<p><strong>Background: </strong>The underlying mechanisms of atherosclerosis and strategies for identifying high cardiovascular risk in psoriasis are incompletely understood. Platelet activity is increased in psoriasis and induces vascular dysfunction. We investigated the platelet phenotype and platelet transcriptome as one potential mechanism to explain cardiovascular risk in psoriasis.</p><p><strong>Methods: </strong>Psoriasis and controls underwent platelet aggregation and activation studies and platelet RNA sequencing to generate a psoriasis platelet transcriptomic score. The relationship between the platelet transcriptomic score and cardiovascular risk was assessed by arterial stiffness, coronary calcium, and longitudinally in an independent cohort of high cardiovascular-risk individuals undergoing lower extremity arterial revascularization.</p><p><strong>Results: </strong>Psoriasis subjects (n=73; median age, 51 years; body surface area of psoriasis, 3%) compared with controls (n=56; median age, 41 years) trended older (<i>P</i>=0.08) and had greater body mass index (<i>P</i>=0.01) and higher hs-CRP (high-sensitivity C-reactive protein) values (<i>P</i>=0.01). Platelet aggregation in response to collagen (<i>P</i>=0.0049) and ADP (<i>P</i>=0.033), and leukocyte-, neutrophil-, and lymphocyte-platelet aggregates (<i>P</i><0.05 for each comparison) were all higher in psoriasis versus controls. Platelet RNA sequencing comparing 51 patients with psoriasis with 39 controls identified 329 upregulated and 345 downregulated genes (<i>P</i><0.05). Pathway analysis identified dysregulated platelet activation, apoptosis, VEGF, interferon, senescence, IL (interleukin)-1, and clotting cascade signaling between psoriasis and controls. Using a phenotypic rank-based scoring methodology, a psoriasis platelet transcriptomic score comprised of 142 genes differentiated psoriasis from controls. This score correlated with arterial stiffness (<i>r</i>=0.26; <i>P</i>=0.031) and coronary calcium (<i>r</i>=0.58; <i>P</i>=0.0069). In a separate cohort of high cardiovascular-risk patients undergoing lower extremity arterial revascularization, the psoriasis platelet transcriptomic score is associated with incident myocardial infarction (adjHR, 3.7 [95% CI, 1.4-10.1]; <i>P</i>=0.015).</p><p><strong>Conclusions: </strong>Platelet aggregation and activation are increased in patients with controlled psoriatic disease, with the platelet transcriptome associated with proinflammatory, proatherothrombotic pathways, and cardiovascular risk. Our results warrant further investigation of platelet involvement promoting heightened cardiovascular disease in psoriasis.</p>","PeriodicalId":8401,"journal":{"name":"Arteriosclerosis, Thrombosis, and Vascular Biology","volume":" ","pages":""},"PeriodicalIF":7.4,"publicationDate":"2025-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144991485","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":"Lp(a) as a Risk Factor for Peripheral Artery Disease: Context Is Everything.","authors":"Marlys L Koschinsky, Michael B Boffa","doi":"10.1161/ATVBAHA.125.322137","DOIUrl":"10.1161/ATVBAHA.125.322137","url":null,"abstract":"<p><p>Elevated plasma concentrations of Lp(a) (lipoprotein(a)) are an independent and causal risk factor for the development of atherosclerotic cardiovascular diseases, including peripheral artery disease (PAD). Although proatherosclerotic, proinflammatory, procalcific, and prothrombotic effects have been attributed to Lp(a), the precise pathogenic mechanisms by which Lp(a) contributes to these disorders are unclear. Moreover, whether Lp(a) contributes in different ways to atherosclerotic cardiovascular diseases in different vascular sites has not been explored. In particular, PAD involves atherosclerotic plaque rupture and subsequent thrombosis in vessels above the knee, but medial arterial calcification leading to vessel stiffness and thrombosis below the knee; the significance of Lp(a) in these contexts is unclear. Elevated Lp(a) is associated with the spectrum of PAD outcomes, including incident claudication, PAD progression, lower limb revascularization, restenosis, major adverse leg events, including limb amputation, and death and hospitalization due to PAD. Overall, elevated Lp(a) is as potent a risk factor for PAD as it is for coronary artery disease. Reducing Lp(a) to mitigate risk of PAD and to treat patients with PAD, therefore, remains a substantial unmet clinical need, although studies are underway to assess the efficacy of RNA-directed Lp(a)-lowering therapies in preventing atherosclerotic cardiovascular disease events. Mounting clinical trials of these therapies to specifically address their effect on PAD events is the next key step.</p>","PeriodicalId":8401,"journal":{"name":"Arteriosclerosis, Thrombosis, and Vascular Biology","volume":" ","pages":"1505-1515"},"PeriodicalIF":7.4,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144793349","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":"Taking a Cellular TRP Around the Lymphatic Collectors.","authors":"Kathleen M Caron","doi":"10.1161/ATVBAHA.125.323058","DOIUrl":"10.1161/ATVBAHA.125.323058","url":null,"abstract":"","PeriodicalId":8401,"journal":{"name":"Arteriosclerosis, Thrombosis, and Vascular Biology","volume":" ","pages":"1519-1520"},"PeriodicalIF":7.4,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144793353","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":"Circulating Protein Mediators Linking Genetically Predicted Smoking to Abdominal Aortic Aneurysm: A Genomic-Proteomic Analysis.","authors":"Shuai Yuan, Samuel Khodursky, Jiawei Geng, Pranav Sharma, Joshua M Spin, Philip S Tsao, Michael G Levin, Scott M Damrauer","doi":"10.1161/ATVBAHA.125.323057","DOIUrl":"10.1161/ATVBAHA.125.323057","url":null,"abstract":"<p><strong>Background: </strong>Smoking is a well-established risk factor for abdominal aortic aneurysm (AAA). However, the molecular pathways underlying this relationship remain poorly understood. This study aimed to identify circulating protein mediators that may explain the association between smoking and AAA.</p><p><strong>Methods: </strong>We conducted a network Mendelian randomization study using summary-level data from the largest available genome-wide association studies. Our primary smoking exposure was the lifetime smoking index, with smoking initiation and cigarettes per day included as supplementary traits. The AAA data set comprised 39 221 cases and 1 086 107 controls. Protein data were sourced from 2 large cohorts: UKB-PPP (the UK Biobank Pharma Proteomics Project), where proteins were measured using the Olink platform in 54 219 individuals, and deCODE, where proteins were measured using the SomaScan platform in 35 559 individuals. Two-sample Mendelian randomization was used to estimate the association between smoking and AAA (β_total) and between smoking and circulating protein levels (β₁). Summary data-based Mendelian randomization was then used to assess the association between smoking-related proteins and AAA risk (β₂). Mediation pathways were identified based on the directionality of effect estimates, and the corresponding mediation effects were quantified.</p><p><strong>Results: </strong>Genetically proxied smoking traits were consistently associated with an increased risk of AAA. The lifetime smoking index was associated with the levels of 543 out of 5764 unique circulating proteins, with 470 of these associations replicated in supplementary analyses using additional smoking traits and protein sources. Among the smoking-related proteins, genetically proxied levels of 22 were associated with AAA risk. Eight mediation pathways were identified, with ADAMTS15 (a disintegrin and metalloproteinase with thrombospondin motifs 15), IL1RN (interleukin-1 receptor antagonist protein), MMP12 (matrix metalloproteinases 12), PGF (placental growth factor), PCSK9 (proprotein convertase subtilisin/kexin type 9), and UXS1 (UDP-glucuronic acid decarboxylase 1) representing key mediators.</p><p><strong>Conclusions: </strong>This study identified numerous circulating proteins that are potentially causally linked to smoking, and 8 of these proteins were found to mediate the association between smoking and AAA risk.</p>","PeriodicalId":8401,"journal":{"name":"Arteriosclerosis, Thrombosis, and Vascular Biology","volume":" ","pages":"1683-1692"},"PeriodicalIF":7.4,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12285744/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144648406","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":"Human Genetic Evidence Does Not Support a Causal Role for Reduced FXI Levels in Heart Failure Pathogenesis-Brief Report.","authors":"Iyas Daghlas, Dipender Gill","doi":"10.1161/ATVBAHA.125.322971","DOIUrl":"10.1161/ATVBAHA.125.322971","url":null,"abstract":"<p><strong>Background: </strong>Coagulation factor XI (FXI) is a promising therapeutic target for preventing thromboembolic disease while preserving hemostasis. However, recent translational and epidemiological findings have raised concerns that lowering FXI levels may increase heart failure risk. To clarify these potential risks, we investigated whether lifelong genetically reduced FXI levels were associated with risk of heart failure and imaging correlates of cardiovascular function.</p><p><strong>Methods: </strong>We used a genome-wide association study of circulating FXI levels in the deCODE cohort (N=35 559) to identify a genetic proxy in the <i>F11</i> gene for circulating FXI levels. To validate this genetic proxy, we examined its associations with positive control thromboembolic diseases and its mechanistic specificity using cardiovascular risk factors unrelated to coagulation. We then obtained genetic associations for the primary outcome of all-cause heart failure (139 533 cases and 1 568 809 controls) and secondary outcomes of heart failure subtypes (up to 42 081 cases), atrial fibrillation (181 446 cases), and magnetic resonance imaging correlates of cardiovascular function (up to 38 251 participants). We performed Mendelian randomization analyses using the Wald ratio method to estimate the association of a lifelong 1-SD reduction in genetically proxied FXI levels on each outcome.</p><p><strong>Results: </strong>We identified an <i>F11</i> variant that reduced circulating FXI levels by 0.33 SD units (<i>P</i><1×10^-200), conferred protection against venous thromboembolism (odds ratio per 1-SD reduction in FXI levels, 0.61 [95% CI, 0.60-0.63]; <i>P</i>=1.85×10^-198), and showed no association with cardiovascular risk factors (<i>P</i>>0.05). Genetically proxied lower FXI levels were not associated with all-cause heart failure (odds ratio, 0.99 [95% CI, 0.96-1.01]; <i>P</i>=0.34), nor with any secondary clinical or radiographic outcomes (all <i>P</i>>0.05).</p><p><strong>Conclusions: </strong>Current human genetic evidence does not support an adverse effect of lower FXI levels on heart failure risk or cardiovascular function. Further studies examining the effect of FXI levels on cardiac events and function are warranted.</p>","PeriodicalId":8401,"journal":{"name":"Arteriosclerosis, Thrombosis, and Vascular Biology","volume":" ","pages":"1664-1669"},"PeriodicalIF":7.4,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144493818","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":"Bone Marrow Farnesoid X Receptor Deficiency Does Not Impact Atherosclerosis Susceptibility in Male Low-Density Lipoprotein Receptor Knockout Mice.","authors":"Menno Hoekstra, Ruud Out, Zhaosha Li, Reeni B Hildebrand, Theo J C Van Berkel, Miranda Van Eck","doi":"10.1161/ATVBAHA.125.322834","DOIUrl":"10.1161/ATVBAHA.125.322834","url":null,"abstract":"","PeriodicalId":8401,"journal":{"name":"Arteriosclerosis, Thrombosis, and Vascular Biology","volume":" ","pages":"1704-1706"},"PeriodicalIF":7.4,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144599253","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}