Atherosclerosis最新文献

{"title":"Intensive lipid-lowering strategies and major cardiovascular events in patients aged ≥65 years: A meta-analysis of randomized trial subgroups","authors":"Armando Oterino ,&nbsp;Rosa Fernández Olmo ,&nbsp;Miriam Martín Toro ,&nbsp;Alberto Cordero","doi":"10.1016/j.atherosclerosis.2026.120714","DOIUrl":"10.1016/j.atherosclerosis.2026.120714","url":null,"abstract":"<div><h3>Background</h3><div>Elderly patients have been underrepresented in trials that evaluated the effect of intensive lipid-lowering therapy (ILLT) on major adverse cardiovascular events (MACE).</div></div><div><h3>Methods</h3><div>We performed an intention-to-treat metanalysis of published data of phase III trials evaluating ILLT efficacy on MACE, mortality, myocardial infarction and stroke.</div></div><div><h3>Results</h3><div>We analyzed 38,089 patients with age ≥65 from 11 trials. ILLT was associated to lower risk of MACE (HR: 0.85 95% CI 0.80-0.88; p &lt; 0.001) and the effect was similar in all the age groups (heterogeneityI² = 37.7%, p = 0.098). The risk reduction of ILLT was significantly higher (p &lt; 0.01) in primary prevention (HR: 0.66 95% CI 0.57-0.77; p &lt; 0.001) as compared to secondary prevention (HR: 0.86 95% CI 0.82-0.91 p &lt; 0.001). Mortality risk reduction was reported in 7 trials but only a non-significant tendency to lower cardiovascular mortality (HR: 0.94 95% CI 0.84-1.05; p = 0.28) and all-cause mortality (HR: 0.94 95% CI0.87-1.02; p = 0.15) was observed; in contrast, ILLT reduced the risk of myocardial infarction (HR: 0.84 95% CI 0.77-0.90; p = 0.001) and stroke (HR: 0.71 95% CI 0.58-0.86; p &lt; 0.001).</div></div><div><h3>Conclusions</h3><div>ILLT reduces the risk of MACE in the elderly. The risk reduction was similar in all age groups and could be even higher in primary prevention.</div></div>","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"415 ","pages":"Article 120714"},"PeriodicalIF":5.7,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147519638","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":"Traditional cardiovascular risk factors and their association with atherosclerotic cardiovascular disease in homozygous familial hypercholesterolemia: A cross-sectional analysis from the HICC registry","authors":"Willemijn AM. Schonck ,&nbsp;G. Kees Hovingh ,&nbsp;Dirk J. Blom ,&nbsp;Tycho Tromp ,&nbsp;Marina Cuchel ,&nbsp;Fahad Alnouri ,&nbsp;Frederick J. Raal ,&nbsp;Jeanine E. Roeters van Lennep ,&nbsp;Akl C. Fahed ,&nbsp;Alberico L. Catapano ,&nbsp;Aeilko H. Zwinderman ,&nbsp;Erik S.G. Stroes ,&nbsp;Laura D'Erasmo ,&nbsp;Laurens F. Reeskamp ,&nbsp;the Homozygous Familial Hypercholesterolemia International Clinical Collaborators","doi":"10.1016/j.atherosclerosis.2026.120717","DOIUrl":"10.1016/j.atherosclerosis.2026.120717","url":null,"abstract":"<div><h3>Background and aims</h3><div>As survival improves in patients with homozygous familial hypercholesterolemia (HoFH), exposure to traditional cardiovascular risk factors may increasingly influence outcomes. This study aimed to determine the prevalence of traditional coronary artery disease (CAD) risk factors—hypertension, diabetes, smoking, and obesity—and their associations with CAD in HoFH.</div></div><div><h3>Methods</h3><div>We performed a cross-sectional analysis of patients enrolled in the HoFH International Clinical Collaborators (HICC) registry (NCT04815005) between February 2016 and December 2024. Logistic regression was used to estimate the association between risk factors and CAD in risk factor propensity score–matched subgroups. Analyses were stratified by sex, on-treatment LDL-C tertiles, and country-income status.</div></div><div><h3>Results</h3><div>Among 912 patients with HoFH (53.3% female; median age 33.0 years), the prevalence of hypertension was 16.5%, diabetes 3.8%, smoking 8.2%, overweight 25.4%, and obesity 17.6%. Cardiovascular risk factors were more frequent in older patients (e.g., hypertension: 25.7% ≥ 30 years vs. 4.3% &lt; 30 years; p &lt; 0.001), in those from high-income countries (17.8% vs. 14.9%; p = 0.011), and in those achieving lower LDL-C levels (24.1% in the lowest vs. 14.6% in the highest LDL-C tertile; p = 0.004). After propensity score matching, hypertension was significantly associated with CAD (OR 1.85; 95%CI 1.11–3.08, p = 0.02), while diabetes, smoking, and obesity were not associated.</div></div><div><h3>Conclusions</h3><div>Despite the dominant role of cumulative LDL-C burden in the development of CAD, our findings indicate an association between hypertension and CAD in HoFH. Although causal inference is limited by the cross-sectional design, these results highlight the importance of proactive identification and management of hypertension in HoFH alongside intensive lipid-lowering therapy.</div></div>","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"415 ","pages":"Article 120717"},"PeriodicalIF":5.7,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147571877","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":"The persistent challenge of medication adherence after myocardial infarction in the real-world: Why compliance keeps taking the hit","authors":"Enzo Emanuele MD, PhD ,&nbsp;Jacques D. Barth MD, PhD","doi":"10.1016/j.atherosclerosis.2026.120695","DOIUrl":"10.1016/j.atherosclerosis.2026.120695","url":null,"abstract":"","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"415 ","pages":"Article 120695"},"PeriodicalIF":5.7,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147740126","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":"Plaque regression: Risk status or ApoB exposure?","authors":"Katharina Lechner ,&nbsp;Benjamin Lechner ,&nbsp;Oliver Weingärtner","doi":"10.1016/j.atherosclerosis.2026.120719","DOIUrl":"10.1016/j.atherosclerosis.2026.120719","url":null,"abstract":"","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"415 ","pages":"Article 120719"},"PeriodicalIF":5.7,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147740202","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":"Erratum to “2025 Focused update of the 2019 ESC/EAS guidelines for the management of dyslipidaemias” [Atherosclerosis, 409, (October 2025), 120479]","authors":"François Mach (ESC Chairperson) ,&nbsp;Konstantinos C. Koskinas (ESC Chairperson) ,&nbsp;Jeanine E. Roeters van Lennep (EAS Chairperson) ,&nbsp;Lale Tokgözoğlu (Task Force Coordinator) ,&nbsp;Lina Badimon ,&nbsp;Colin Baigent ,&nbsp;Marianne Benn ,&nbsp;Christoph J. Binder ,&nbsp;Alberico L. Catapano ,&nbsp;Guy G. De Backer ,&nbsp;Victoria Delgado ,&nbsp;Natalia Fabin ,&nbsp;Brian A. Ference ,&nbsp;Ian M. Graham ,&nbsp;Ulf Landmesser ,&nbsp;Ulrich Laufs ,&nbsp;Borislava Mihaylova ,&nbsp;Børge Grønne Nordestgaard ,&nbsp;Dimitrios J. Richter ,&nbsp;Marc S. Sabatine","doi":"10.1016/j.atherosclerosis.2026.120703","DOIUrl":"10.1016/j.atherosclerosis.2026.120703","url":null,"abstract":"","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"415 ","pages":"Article 120703"},"PeriodicalIF":5.7,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147600189","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":"Achieving LDL-C <1.0 mmol/L and cardiovascular outcomes in patients with coronary artery disease who received percutaneous coronary intervention","authors":"Yu Kataoka ,&nbsp;Stephen J. Nicholls ,&nbsp;Satoshi Kitahara ,&nbsp;Aya Katasako-Yabumoto ,&nbsp;Hayato Hosoda ,&nbsp;Sayaka Funabashi ,&nbsp;Kentaro Mitsui ,&nbsp;Kota Murai ,&nbsp;Takamasa Iwai ,&nbsp;Kenichiro Sawada ,&nbsp;Hideo Matama ,&nbsp;Satoshi Honda ,&nbsp;Kensuke Takagi ,&nbsp;Masashi Fujino ,&nbsp;Shuichi Yoneda ,&nbsp;Fumiyuki Otsuka ,&nbsp;Kazuhiro Nakao ,&nbsp;Yasuhide Asaumi ,&nbsp;Teruo Noguchi","doi":"10.1016/j.atherosclerosis.2026.120684","DOIUrl":"10.1016/j.atherosclerosis.2026.120684","url":null,"abstract":"<div><h3>Background and aims</h3><div>The ESC guideline recommends LDL-C&lt;1.0 mmol/L in extreme-risk patients. However, recent clinical trials demonstrated cardiovascular benefits with achieving very low LDL-C levels even in very high-risk patients including patients with CAD. Patients with CAD may more benefit from lowering LDL-C&lt;1.0 mmol/L rather than their guideline-recommended LDL-C goal (&lt;1.4 mmol/L).</div></div><div><h3>Methods</h3><div>The current multi-center observational study analyzed 2560 patients with CAD receiving PCI (2017.1.1-2022.8.31). All of study participants were clinically followed for at least three years after PCI. The primary (cardiac death, non-fatal MI and clinically-driven coronary revascularization at non-culprit segments) and secondary outcomes (cardiac death, non-fatal MI) were compared in those stratified according to on-treatment LDL-C levels at 2 months after PCI (&lt;1.0, 1.0-1.3 and ≥ 1.4 mmol/L).</div></div><div><h3>Results</h3><div>On-treatment LDL-C&lt;1.0 mmol/L was achieved in 9.8% (=251/2560) of study participants. In extreme-risk patients exhibiting the concomitance of polyvascular disease or a history of recurrent ASCVD, the proportions of LDL-C&lt;1.0 mmol/L were 10.5 and 9.6%, respectively. More intensified lipid-lowering therapies were used in those with on-treatment LDL-C&lt;1.0 mmol/L (high-intensity statin = 77.7%, p &lt; 0.001; ezetimibe = 67.3%, p &lt; 0.001; PCSK9–I = 13.9%, p &lt; 0.001). During the observational perid (median = 1882 days), achieving on-treatment LDL-C&lt;1.0 mmol/L significantly reduced risks of primary (adjusted HR = 0.23, 95%CI = 0.11-0.48, p &lt; 0.001) and secondary outcomes (adjusted HR = 0.31, 95%CI = 0.11-0.84, p = 0.022). These benefits were consistently observed regardless of age, gender, types of CAD and various traditional risk factors.</div></div><div><h3>Conclusions</h3><div>Achieving LDL-C&lt;1.0 mmol/L mitigated risks of subsequent atherosclerotic cardiovascular events in patients with CAD. More actions are needed to further promote the intensification of lipid-lowering therapies in patients with CAD.</div></div>","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"415 ","pages":"Article 120684"},"PeriodicalIF":5.7,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147589560","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":"Genetically proxied IL-6 signaling inhibition, lipoprotein(a) levels, and atherosclerotic disease risk","authors":"Iyas Daghlas ,&nbsp;Marios K. Georgakis ,&nbsp;Stephen O. Brennan ,&nbsp;Benoit J. Arsenault ,&nbsp;Stephen Burgess ,&nbsp;Dipender Gill","doi":"10.1016/j.atherosclerosis.2026.120723","DOIUrl":"10.1016/j.atherosclerosis.2026.120723","url":null,"abstract":"<div><h3>Background</h3><div>Clinical trials have shown that interleukin-6 (IL-6) signaling inhibitors reduce lipoprotein(a) [Lp(a)] levels, though the relevance of this reduction to atherosclerotic cardiovascular disease (ASCVD) risk is uncertain. We leveraged Mendelian randomization (MR) to investigate the extent to which Lp(a) reduction mediates the effects of IL-6 signaling inhibition on ASCVD.</div></div><div><h3>Methods</h3><div>IL-6 signaling inhibition was proxied by the <em>IL6R</em> variant p.Asp358Ala and scaled to C-reactive protein (CRP) levels. Genetic associations with Lp(a) were obtained from UK Biobank (n = 343,681). Outcomes included large-artery atherosclerotic stroke (LAAS: 6399 cases), carotid plaque (29,760 cases), and coronary artery disease (CAD: 181,522 cases). MR analyses estimated the association of IL-6 signaling inhibition with Lp(a) and ASCVD, and we quantified the proportion of the IL-6–ASCVD association mediated by Lp(a). Individual-level analyses tested whether effects of IL-6 signaling inhibition on Lp(a) and CAD were amplified in carriers of Lp(a)-raising variants.</div></div><div><h3>Results</h3><div>Genetically proxied IL-6 signaling inhibition modestly reduced Lp(a) (−3.01 mg/dL per 1-ln(CRP) reduction, 95% CI -4.79, −1.23) and protected against all ASCVD outcomes (ORs: 0.34-0.69). Lp(a) mediated only a small proportion of the IL-6–ASCVD association (range: 1.3%-4.8%). In carriers of Lp(a)-raising variants, the IL-6–Lp(a) association was stronger (−9.8 mg/dL, 95% CI -14.6, −5.1; <em>p</em>_{<em>interaction</em>} = 6.38 × 10⁻⁷), though IL-6–CAD associations were similar (<em>p</em>_{<em>interaction</em>} = 0.75) and the proportion mediation remained low (4.2%-15.6%).</div></div><div><h3>Conclusions</h3><div>These findings suggest that Lp(a) minimally mediates and does not modify the cardiovascular benefits of IL-6 signaling inhibition, supporting these targets as independent and complementary for ASCVD. The amplified IL-6–Lp(a) association in carriers of Lp(<em>a</em>)-raising variants warrants replication.</div></div>","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"415 ","pages":"Article 120723"},"PeriodicalIF":5.7,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147600201","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":"Risk factors for atherosclerotic cardiovascular disease in individuals with heterozygous familial hypercholesterolemia: a systematic review and meta-analysis","authors":"María Elena Mansilla-Rodríguez ,&nbsp;José Luis Sánchez-Ramos ,&nbsp;Alina Rigabert Sánchez-Junco ,&nbsp;Jing Pang ,&nbsp;Dick C. Chan ,&nbsp;Eva Nadiejda Gutiérrez-Cortizo ,&nbsp;Pedro Mata ,&nbsp;Gerald F. Watts ,&nbsp;Manuel Jesús Romero-Jiménez","doi":"10.1016/j.atherosclerosis.2026.120650","DOIUrl":"10.1016/j.atherosclerosis.2026.120650","url":null,"abstract":"<div><h3>Background and aims</h3><div>Familial hypercholesterolemia (FH) is a highly prevalent monogenic disorder characterized by elevated low-density lipoprotein-cholesterol (LDL-C) levels and premature atherosclerotic cardiovascular disease (ASCVD). The risk factors associated with cardiovascular events in this population vary considerably among studies. This systematic review aims to identify the key risk factors predicting cardiovascular events in patients with a confirmed genetic diagnosis of heterozygous FH (PROSPERO, CRD42022304273).</div></div><div><h3>Methods and analysis</h3><div>Cochrane Library, Embase, MEDLINE, Scopus, UpToDate and other literature databases were searched from inception to June 2023. Records were eligible if they included studies reporting risk factors for ASCVD endpoints in adult patients with a genetic diagnosis of FH. A meta-analysis was performed using MetaEasy.</div></div><div><h3>Results</h3><div>A total of 21 studies were identified, involving 23,613 individual participants and 3489 prevalent cardiovascular events. The sex distribution was 47.2% male and 52.8% female. Most of the studies were conducted in European populations, representing 90.5% of the total. The meta-analysis found associations between ASCVD and hypertension (effect size 0.414; 95% CI: 0.346-0.482), male sex (0.334; 0.213-0.456), smoking (0.324; 0.203-0.445), lipoprotein(a) (0.219; 0.127-0.312), age (0.212; 0.161-0.264), body mass index (0.108; 0.028-0.188), triglycerides (0.084; 0.057-0.111) and LDL-C (0.015; 0.002-0.028).</div></div><div><h3>Conclusions</h3><div>This is the first systematic review and meta-analysis demonstrating that hypertension, male sex, smoking, lipoprotein(a), age, body mass index, triglycerides and LDL-C are significantly and independently associated with ASCVD in genetically confirmed patients with heterozygous FH. These data can inform risk stratification models and optimise therapy in such patients.</div></div>","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"415 ","pages":"Article 120650"},"PeriodicalIF":5.7,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147740136","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":"Hypertension, smoking and adiposity: old enemies, new priorities in FH","authors":"Arturo Cesaro MD, PhD ,&nbsp;Paolo Calabrò MD, PhD ,&nbsp;Stefano Romeo MD, PhD","doi":"10.1016/j.atherosclerosis.2026.120702","DOIUrl":"10.1016/j.atherosclerosis.2026.120702","url":null,"abstract":"","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"415 ","pages":"Article 120702"},"PeriodicalIF":5.7,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147740127","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":"Cell surface nucleolin promotes endothelial cell pyroptosis in atherosclerosis through RASSF2","authors":"Li Fang,&nbsp;Zhijie Shen,&nbsp;Dan Huang,&nbsp;Chenyu Lou,&nbsp;Yalan Yu,&nbsp;Yuli Lin,&nbsp;Yinzhuang Zhang","doi":"10.1016/j.atherosclerosis.2026.120715","DOIUrl":"10.1016/j.atherosclerosis.2026.120715","url":null,"abstract":"<div><h3>Background and aims</h3><div>Increasing evidence indicates that modulating pyroptosis in endothelial cells (ECs) can alleviate atherosclerosis (AS) progression; however, despite reports that nucleolin (NCL) regulates vascular smooth muscle cell proliferation in AS, the potential mechanism by which cell surface NCL mediates pyroptosis in ECs during AS remains poorly understood.</div></div><div><h3>Methods</h3><div>AS was induced in ApoE^−/− mice by feeding a high-fat diet, after which aortic lesions were evaluated. Pyroptosis, inflammatory status, and NCL expression in ECs of the aortic root were then assessed. The effects of NLRP3 inflammasome inhibition and NCL modulation on atherosclerotic lesion severity in AS mice, as well as on pyroptosis in ox-LDL-stimulated ECs, were systematically investigated. In addition, the mechanistic role of NCL in AS was further explored using approaches including immunoprecipitation-mass spectrometry (IP-MS).</div></div><div><h3>Results</h3><div>AS model mice developed severe aortic lesions accompanied by pronounced EC pyroptosis and inflammation, together with elevated NCL expression in ECs of the aortic root. Both inhibition of NLRP3 and NCL knockdown alleviated atherosclerotic lesion severity in ApoE^−/− mice and attenuated ox-LDL-induced EC pyroptosis. Mechanistically, cell-surface NCL interacted with RASSF2 via its RNA-binding domain, and suppression of NCL decreased nuclear RASSF2 expression. NCL facilitated the translocation of RASSF2 into the nucleus, thereby exacerbating EC pyroptosis and amplifying inflammatory responses.</div></div><div><h3>Conclusions</h3><div>This study demonstrates that, in AS, NCL exacerbates EC pyroptosis and promotes disease progression by facilitating nuclear transport of RASSF2. This study defines the mechanistic roles of NCL in AS, thereby identifying a new molecular pathway and suggesting potential therapeutic targets.</div></div>","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"415 ","pages":"Article 120715"},"PeriodicalIF":5.7,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147525671","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}