Atherosclerosis最新文献

{"title":"PlGF modulates vascular smooth muscle cells phenotype to enhance atherosclerotic plaque stability.","authors":"Jing Li, Qianyi Yu, Jianrong Bao, Zhigang Sun, Li Hou, Jun Zhang, Bo Song, Lei Sun, Xiao Yu","doi":"10.1016/j.atherosclerosis.2026.121929","DOIUrl":"https://doi.org/10.1016/j.atherosclerosis.2026.121929","url":null,"abstract":"<p><strong>Background and aims: </strong>Phenotypic switching of vascular smooth muscle cells (VSMCs) is critical for determining atherosclerotic plaque stability; however, the mechanisms that drive a stability-promoting VSMCs phenotype remain unclear. While clinical evidence associates high placental growth factor (PlGF) expression with stable advanced plaques, the underlying pathways are undefined. This study investigates the mechanism by which PlGF regulates VSMCs phenotypic switching to enhance plaque stability.</p><p><strong>Methods: </strong>PlGF expression was quantified in human carotid plaques by immunohistochemistry. Atherosclerosis was induced in ApoE^-/- mice fed a high-fat diet, followed by PlGF administration for 7 days. Plaque size, composition, and the expression of PlGF, Flt-1, CD209/CD163, TGF-β1, α-SMA and CD68 were assessed at 14 and 28 days by immunohistochemistry/immunofluorescence. In vitro, flow cytometry, Western blot, ELISA and conditioned co-culture systems evaluated macrophage polarization, TGF-β1 secretion, and effects on human carotid VSMCs phenotype.</p><p><strong>Results: </strong>PlGF was elevated in stable human plaques, co-localized with α-SMA in fibrous cap and shoulder regions. In PlGF-treated mice, PlGF, α-SMA and TGF-β1 increased in the fibrous cap and shoulder regions of plaques, while aortic root plaque area decreased. Co-localization of Flt-1/CD209 and TGF-β1/CD209 was enhanced, with TGF-β1/CD209 exceeding TGF-β1/α-SMA. Mechanistically, PlGF polarized macrophages toward an anti-inflammatory phenotype, increasing TGF-β1 secretion, which upregulated α-SMA in VSMCs.</p><p><strong>Conclusions: </strong>This study identifies a PlGF/anti-inflammatory macrophage/TGF-β1/contractile VSMCs signaling axis that reinforces fibrous cap integrity and promotes plaque stability in advanced atherosclerosis.</p>","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"422 ","pages":"121929"},"PeriodicalIF":7.1,"publicationDate":"2026-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149223043","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Beyond a single measurement: the role of cumulative LDL-C exposure after percutaneous coronary intervention.","authors":"Pompilio Faggiano, Giacomo Gamberini, Andrea Faggiano","doi":"10.1016/j.atherosclerosis.2026.121926","DOIUrl":"https://doi.org/10.1016/j.atherosclerosis.2026.121926","url":null,"abstract":"","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":" ","pages":"121926"},"PeriodicalIF":7.1,"publicationDate":"2026-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149222957","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Lp(a) reduction with PCSK9 inhibitors: How does real-world data stack up?","authors":"Karam Kostner","doi":"10.1016/j.atherosclerosis.2026.121928","DOIUrl":"https://doi.org/10.1016/j.atherosclerosis.2026.121928","url":null,"abstract":"","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":" ","pages":"121928"},"PeriodicalIF":7.1,"publicationDate":"2026-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149179278","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cumulative LDL cholesterol exposure after percutaneous coronary intervention is associated with major adverse cardiovascular events.","authors":"Shigetaka Kageyama, Hirofumi Sugiyama, Koichiro Murata, Ryuzo Nawada, Tomoya Onodera, Yuichiro Maekawa","doi":"10.1016/j.atherosclerosis.2026.121900","DOIUrl":"https://doi.org/10.1016/j.atherosclerosis.2026.121900","url":null,"abstract":"<p><strong>Background and aims: </strong>We assessed whether AUC-derived cumulative low-density lipoprotein cholesterol (LDL-C) exposure after percutaneous coronary intervention (PCI) was associated with subsequent major adverse cardiac and cerebrovascular events (MACCE), and compared this longitudinal metric with the latest LDL-C measurement.</p><p><strong>Methods: </strong>We conducted a retrospective, single-centre, matched case-control study of consecutive patients undergoing successful PCI from 2010 to 2020. Cases with major adverse cardiac and cerebrovascular events (MACCE) were matched 1:1 to event-free controls by follow-up duration. Cumulative LDL-C exposure was calculated from serial LDL-C measurements by the trapezoidal rule. Conditional logistic regression with restricted cubic splines was used, with prespecified multivariable adjustment for available baseline clinical characteristics.</p><p><strong>Results: </strong>Among 544 matched pairs, cumulative LDL-C exposure was higher in MACCE cases than controls (median 489.8 vs 179.5 mg/dL·year; p < 0.001), whereas the latest LDL-C was modestly lower in cases (74.3 ± 26.6 vs 81.2 ± 26.4 mg/dL; p < 0.001). In the multivariable-adjusted spline model, the odds ratio at 400 mg/dL·year was 2.73 (95% CI, 2.24-3.32) relative to the median exposure in controls. Associations were consistent in time-truncated and component-specific exploratory analyses.</p><p><strong>Conclusions: </strong>In secondary prevention after PCI, AUC-derived cumulative LDL-C exposure was associated with MACCE beyond available baseline clinical characteristics and may complement snapshot LDL-C assessment. The apparent 400 mg/dL·year range is exploratory and hypothesis-generating, not a clinically actionable treatment target.</p>","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":" ","pages":"121900"},"PeriodicalIF":7.1,"publicationDate":"2026-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149007839","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"What does focal coronary imaging tell us about the whole patient?","authors":"Stephen J Nicholls","doi":"10.1016/j.atherosclerosis.2026.121904","DOIUrl":"https://doi.org/10.1016/j.atherosclerosis.2026.121904","url":null,"abstract":"","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":" ","pages":"121904"},"PeriodicalIF":7.1,"publicationDate":"2026-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149029827","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mapping the modifiable exposome for ischemic stroke: association, causality, and preventive potential","authors":"Manqi Zheng,&nbsp;Qin Xu,&nbsp;Xue Xia,&nbsp;Meng Gao,&nbsp;Jing Li,&nbsp;Xiaoyan Huang,&nbsp;Anxin Wang","doi":"10.1016/j.atherosclerosis.2026.120693","DOIUrl":"10.1016/j.atherosclerosis.2026.120693","url":null,"abstract":"<div><h3>Background and aims</h3><div>Previous hypothesis-driven studies focused on limited risk factors for ischemic stroke (IS) with inconsistent findings. We aimed to systematically identify modifiable factors, assess causality, quantify joint impact, and evaluate public health implications of conservative versus radical multi-domain IS intervention strategies.</div></div><div><h3>Methods</h3><div>We conducted a large prospective cohort study using UK Biobank and a bidirectional two-sample Mendelian randomization study. Exposures included 323 modifiable factors in seven domains: early life, health and medical history, lifestyle, local environment, physical measures, psychosocial factors, and sociodemographics. Exposome-wide association scan was used to investigate the associations between exposures and IS onset, and multivariable Cox models to assess their joint impact. Weighted population attributable fraction was estimated by partially eliminating exposures.</div></div><div><h3>Results</h3><div>497,856 IS-free UK adults were enrolled during 2006-2010, and 10,593 experienced IS with a median follow-up of 14.53 years. Among 68 modifiable factors significantly associated with IS, 18 demonstrated robust causality. Controlling for the overlapping hazards of exposures, worsening risk profiles in each domain independently increased IS risk. Eradicating all modifiable risk factors would prevent 72.21% (95% CI 69.37%-74.83%) of IS, whereas a one-third reduction in the exposure levels of modifiable factors would prevent 68.19% (95% CI 64.22%-71.81%). These findings remained consistent across populations stratified by age, sex, and polygenic risk score-based genetic risk.</div></div><div><h3>Conclusions</h3><div>This hypothesis-free and triangulated study provided comprehensive information on the modifiable exposome for IS. Our findings suggested that a moderate reduction in risk factor exposure achieved a preventive impact comparable to total eradication, supporting the potential for efficient public health strategies.</div></div>","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"420 ","pages":"Article 120693"},"PeriodicalIF":7.1,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148839127","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Methodological and clinical considerations in a Japanese cohort study of familial hypercholesterolemia and stroke","authors":"Yining Hui,&nbsp;Gang Tian","doi":"10.1016/j.atherosclerosis.2026.120753","DOIUrl":"10.1016/j.atherosclerosis.2026.120753","url":null,"abstract":"","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"419 ","pages":"Article 120753"},"PeriodicalIF":7.1,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147810154","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"EFFICACY AND SAFETY OF LERODALCIBEP, A NOVEL THIRD GENERATION PCSK9 INHIBITOR, IN SUBJECTS WITH SEVERE LDL-C ELEVATIONS COMPLETING THE 124-WEEK OPEN-LABEL PHASE 3 EXTENSION STUDY","authors":"David Kallend,&nbsp;Frederick Raal,&nbsp;Nyda Fourie,&nbsp;Russell Scott,&nbsp;Miriam Anderson,&nbsp;Jeffrey Vest,&nbsp;Evan Stein","doi":"10.1016/j.atherosclerosis.2026.120862","DOIUrl":"10.1016/j.atherosclerosis.2026.120862","url":null,"abstract":"","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"419 ","pages":"Article 120862"},"PeriodicalIF":7.1,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148924408","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"LDL RECEPTOR-MEDIATED UPTAKE OF LIPOPROTEINS FUELS HUMAN CD4+ T CELL POLARIZATION TOWARDS A C-MAF-IL-10 AND FOXP3-DRIVEN REGULATORY PHENOTYPE","authors":"Angela Markovska,&nbsp;Niels Van Heusden,&nbsp;Enric Mocholi,&nbsp;Edwin Stigter,&nbsp;Can Gulersonmez,&nbsp;Sander Kooijman,&nbsp;Leonie Van Der Zee,&nbsp;Monique Mulder,&nbsp;Jeanine Roeters Van Lennep,&nbsp;Patrick Rensen,&nbsp;Jorg Van Loosdregt,&nbsp;Sebastiaan Vastert,&nbsp;Noam Zelcer,&nbsp;Marianne Boes,&nbsp;Henk Schipper","doi":"10.1016/j.atherosclerosis.2026.120896","DOIUrl":"10.1016/j.atherosclerosis.2026.120896","url":null,"abstract":"","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"419 ","pages":"Article 120896"},"PeriodicalIF":7.1,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148924417","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CARDIOPROTECTIVE GLUCOSE-LOWERING DRUGS, STATINS, AND SECONDARY MAJOR ADVERSE CARDIO-VASCULAR EVENTS","authors":"Tummas Ternhamar,&nbsp;Mia Johansen,&nbsp;Borge Nordestgaard,&nbsp;Shoaib Afzal","doi":"10.1016/j.atherosclerosis.2026.120848","DOIUrl":"10.1016/j.atherosclerosis.2026.120848","url":null,"abstract":"","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"419 ","pages":"Article 120848"},"PeriodicalIF":7.1,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148915905","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}