Atherosclerosis最新文献

{"title":"The “SMART” side of hypertriglyceridemia","authors":"M. Castro Cabezas , B. Klop","doi":"10.1016/j.atherosclerosis.2025.120467","DOIUrl":"10.1016/j.atherosclerosis.2025.120467","url":null,"abstract":"","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"408 ","pages":"Article 120467"},"PeriodicalIF":5.7,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144759027","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":"Making the invisible visible: Leveraging electronic health records to uncover familial hypercholesterolemia in primary care","authors":"Meral Kayikcioglu","doi":"10.1016/j.atherosclerosis.2025.120454","DOIUrl":"10.1016/j.atherosclerosis.2025.120454","url":null,"abstract":"","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"408 ","pages":"Article 120454"},"PeriodicalIF":5.7,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144726957","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":"Reply to: “Does statin matter when it comes to Lipoprotein(a) levels?”","authors":"Sining Xie , Federica Galimberti , Elena Olmastroni , Stefano Carugo , Alberico L. Catapano , Manuela Casula , META-LIPID Group","doi":"10.1016/j.atherosclerosis.2025.120465","DOIUrl":"10.1016/j.atherosclerosis.2025.120465","url":null,"abstract":"","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"408 ","pages":"Article 120465"},"PeriodicalIF":5.7,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144752219","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":"Pressure- and flow-driven biomechanical factors and carotid atherosclerosis","authors":"Johann Auer MD, FESC, FACC, FAHA, FSACI , Paul F. Harbich , Julia Auer , Lisa Auer","doi":"10.1016/j.atherosclerosis.2025.120444","DOIUrl":"10.1016/j.atherosclerosis.2025.120444","url":null,"abstract":"","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"408 ","pages":"Article 120444"},"PeriodicalIF":5.7,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144641630","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":"Adenylate kinase 4 (AK4) deficiency prevents vascular smooth muscle cell phenotypic switching by regulating mitochondrial dysfunction through AMPKα inactivation","authors":"Shu-Min Zhang ,&nbsp;Hanshen Luo ,&nbsp;Zuozhi Li ,&nbsp;Mingzhao Du ,&nbsp;Jingjie Chen ,&nbsp;Ding-Sheng Jiang ,&nbsp;Yuying Zhang ,&nbsp;Chunping Li ,&nbsp;Xuanyue Yang ,&nbsp;Xue-Sheng Wang ,&nbsp;Ze-Min Fang ,&nbsp;Fu-Han Gong ,&nbsp;Jianye Yang","doi":"10.1016/j.atherosclerosis.2025.120399","DOIUrl":"10.1016/j.atherosclerosis.2025.120399","url":null,"abstract":"<div><h3>Background and aims</h3><div><span><span>Mitochondrial dynamics are key mechanism regulating the conversion of </span>vascular smooth muscle cells<span> (VSMCs) from a contractile to a synthetic phenotype, which is involved in neointima formation and </span></span>restenosis. However, the underlying mechanisms leading to mitochondrial dysfunction are not fully understood.</div></div><div><h3>Methods</h3><div>Western blot<span><span> was used to detect the expression of relevant molecules at the protein level. CCK-8, EdU assays, and transwell were used to test </span>cell proliferation<span> and migration capacity. Flow cytometry was used to assess cell cycle and ROS.</span></span></div></div><div><h3>Results</h3><div><span><span>AK4 was upregulated in 10 % </span>fetal bovine serum<span><span><span> (FBS)- and 20 ng/mL platelet-derived growth factor-BB (PDGF-BB)-induced human aortic VSMCs (HASMCs). Knockdown of AK4<span> suppressed the proliferation and synthetic phenotype of HASMCs, while AK4<span> overexpression accelerated it. Mechanistically, AK4 interacted with </span></span></span>protein kinase AMP-activated catalytic </span>subunit alpha<span> (AMPKα) and promoted the phosphorylation of AMPKα<span><span><span><span> at Thr172, which reduced mitochondrial oxidative damage and improved mitochondrial function. Furthermore, activation of </span>AMPKα by </span>metformin or </span>AICAR<span> (acadesine) reversed the inhibitory effects of AK4 deficiency on HASMC phenotypic switching. Moreover, overexpression of wild-type AMPKα<span> counteracted the effects of AK4 knockdown, whereas mutational inactivation of AMPKα (AMPKα</span></span></span></span></span></span>^T172A) was not effective in reversing the effect on HASMCs.</div></div><div><h3>Conclusions</h3><div>Our findings suggest that AK4 is a novel regulator of AMPKα activity<span> and positively regulates VSMC dedifferentiation<span><span>, proliferation, and migration. Targeted inhibition of AK4 may be a potential approach for the treatment of neointima formation and </span>restenosis.</span></span></div></div>","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"408 ","pages":"Article 120399"},"PeriodicalIF":5.7,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144282245","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 stenosis: Is CT enough to assess the vulnerable carotid plaque?","authors":"Edoardo Conte MD","doi":"10.1016/j.atherosclerosis.2025.120422","DOIUrl":"10.1016/j.atherosclerosis.2025.120422","url":null,"abstract":"","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"408 ","pages":"Article 120422"},"PeriodicalIF":5.7,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144607260","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":"Twist1 promoting neointima hyperplasia after vascular injury in diabetes via regulating hyperglycemia-induced phenotype switching of vascular smooth muscle cells","authors":"Yaoling Wang ,&nbsp;Kang Yang ,&nbsp;Gege Jiang ,&nbsp;Xichuan Zheng ,&nbsp;Fang Cheng ,&nbsp;Wei Li","doi":"10.1016/j.atherosclerosis.2025.120496","DOIUrl":"10.1016/j.atherosclerosis.2025.120496","url":null,"abstract":"<div><h3>Background and aims</h3><div>Neointimal hyperplasia is a key pathology in Type 2 Diabetes Mellitus (T2DM) vascular complications. It involves phenotypic switching of vascular smooth muscle cells (VSMCs) triggered by hyperglycemia, though the exact mechanisms remain unclear.</div></div><div><h3>Methods</h3><div>We employed Twist1 vascular smooth muscle-specific knockout mice with carotid artery ligation in a T2DM model to study Twist1's role in diabetic neointimal hyperplasia. In vitro, we examined how hyperglycemia via Pkcβ/Ikkβ/Nf-κb pathway affects Twist1's regulation of contractile proteins, matrix molecules, cell morphology, migration, and proliferation in rat VSMCs using Western blotting, immunofluorescence, wound healing assays, and EdU incorporation. Co-immunoprecipitation and colocalization assessed how Twist1-p300 interaction under high glucose affects Myocardin-Srf binding.</div></div><div><h3>Results</h3><div>Twist1 was significantly upregulated in VSMCs of T2DM mice. Vascular smooth muscle-specific Twist1 knockout reduced neointimal formation after vascular injury in T2DM. High glucose activated Pkcβ/Ikkβ/Nf-κb pathway, promoting Twist1 upregulation and nuclear translocation, decreasing contractile protein expression while increasing matrix molecules and VSMC proliferation/migration. Mechanistically, upregulated Twist1 increased p300 binding, blocking p300's transcriptional co-activation of Myocardin/Srf and inhibiting contractile gene transcription in VSMCs.</div></div><div><h3>Conclusions</h3><div>Hyperglycemia activates the PKCβ/IKKβ/NF-κB pathway, upregulating Twist1 and promoting its nuclear translocation. Twist1 binding to p300 inhibits Myocardin/SRF-mediated contractile gene transcription, leading to VSMC phenotypic switching and neointimal hyperplasia. These findings highlight Twist1 as a potential therapeutic target for diabetic vascular complications.</div></div>","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"409 ","pages":"Article 120496"},"PeriodicalIF":5.7,"publicationDate":"2025-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144903299","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":"Understanding MASLD — from molecular pathogenesis to cardiovascular risk: A concise review for the clinical cardiologist","authors":"Carlo Ratti ,&nbsp;Mattia Malaguti ,&nbsp;D'Aniello Emanuele ,&nbsp;Antonio Bellasi ,&nbsp;Gianluca Sanna","doi":"10.1016/j.atherosclerosis.2025.120495","DOIUrl":"10.1016/j.atherosclerosis.2025.120495","url":null,"abstract":"<div><h3>Background and aims</h3><div>Metabolic dysfunction-associated steatotic liver disease (MASLD) has recently replaced non-alcoholic fatty liver disease (NAFLD) as the preferred nomenclature, reflecting a shift toward inclusion-based diagnostic criteria rooted in metabolic dysfunction. Beyond its hepatic implications, MASLD has emerged as an independent, modifiable driver of cardiovascular disease (CVD).</div></div><div><h3>Methods</h3><div>This review summarizes and synthesizes robust epidemiological and mechanistic evidence linking MASLD to cardiovascular outcomes.</div></div><div><h3>Results</h3><div>MASLD is associated with increased risk of coronary artery disease, myocardial infarction, atrial fibrillation, stroke, and heart failure—particularly heart failure with preserved ejection fraction (HFpEF). Shared pathophysiological mechanisms include insulin resistance, chronic inflammation, oxidative stress, endothelial dysfunction, and atherogenic dyslipidemia, which collectively contribute to both hepatic fibrogenesis and vascular injury. Fibrosis stage, the strongest predictor of hepatic outcomes, also correlates with subclinical atherosclerosis and cardiovascular mortality, yet remains unaccounted for in current CVD risk models. Non-invasive fibrosis markers such as FIB-4 and elastography, originally developed for hepatology, are gaining traction in cardiovascular risk stratification. Furthermore, pharmacologic agents such as GLP-1 receptor agonists and SGLT2 inhibitors demonstrate dual efficacy in improving hepatic, metabolic, and cardiovascular outcomes.</div></div><div><h3>Conclusions</h3><div>This review provides an updated synthesis for cardiologists, outlining the evolution of MASLD nomenclature, its systemic pathophysiology, and its clinical implications—underscoring the urgent need for integrated, multidisciplinary management of this underrecognized cardiometabolic disease.</div></div>","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"409 ","pages":"Article 120495"},"PeriodicalIF":5.7,"publicationDate":"2025-08-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144907900","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":"Cardiac macrophages and their functions in homeostasis and injury","authors":"Giulia Trimaglio ,&nbsp;Peter Mirtschink ,&nbsp;Ali El-Armouche ,&nbsp;Triantafyllos Chavakis","doi":"10.1016/j.atherosclerosis.2025.120480","DOIUrl":"10.1016/j.atherosclerosis.2025.120480","url":null,"abstract":"<div><div>Due to their remarkable plasticity, macrophages can adapt to diverse environments and challenges therein, thereby exerting tissue-specific and context-specific functions. Macrophages are the most frequent immune cell population present in the heart and contribute substantially to cardiac homeostasis and function. Moreover, macrophages are key regulators throughout all stages of heart injury, acquiring diverse phenotypes that can either ameliorate or exacerbate cardiac pathology in a context-dependent manner. The contribution of macrophages to both tissue damage as well as to recovery/tissue repair during heart injury provides avenues for therapeutic modulation of their functions to beneficially influence heart injury progression and hence prevent heart failure. However, to effectively fine-tune macrophage function, a deep understanding of their heterogeneity is required. The present review focuses on the phenotypic diversity and different roles of macrophages in cardiac homeostasis as well as in ischemic and non-ischemic heart disease, and discusses macrophages as potential therapeutic targets in the settings of heart injury.</div></div>","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"409 ","pages":"Article 120480"},"PeriodicalIF":5.7,"publicationDate":"2025-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144996285","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":"Sex differences in cholesterol levels among prepubertal children.","authors":"Jan Kafol, Mia Becker, Barbara Cugalj Kern, Jaka Sikonja, Matej Mlinaric, Katarina Sedej, Matej Kafol, Ana Drole Torkar, Jernej Kovac, Tadej Battelino, Urh Groselj","doi":"10.1016/j.atherosclerosis.2025.120484","DOIUrl":"https://doi.org/10.1016/j.atherosclerosis.2025.120484","url":null,"abstract":"<p><strong>Background and aims: </strong>Sex differences in cholesterol levels are well documented in adults and adolescents, but limited data exist for prepubertal children. This study aimed to evaluate innate sex differences in total cholesterol (TC) and low-density lipoprotein cholesterol (LDL-C) levels among prepubertal children, both in the general population and among those with familial hypercholesterolemia (FH).</p><p><strong>Methods: </strong>This cross-sectional study used data from Slovenia's Universal FH Screening Program. Two population-based random samples of children undergoing routine cholesterol screening at age 5 years were included from 2014 (N = 3412) and 2023 (N = 4182). In addition, a referred cohort from the Slovenian Hypercholesterolemia Registry (n = 1160, aged <10 years) who underwent genetic testing was analyzed.</p><p><strong>Results: </strong>In both the 2014 and 2023 cohorts, girls had significantly higher TC levels than boys (median difference: 0.10-0.11 mmol/L; p < 0.05). Among FH-negative children in the Registry, girls had on average 0.14 mmol/L higher TC and 0.13 mmol/L higher LDL-C than boys (both p < 0.05). No sex differences were observed in FH-positive children (p = 0.83 for TC; p = 0.82 for LDL-C). In the overall Registry cohort, after adjusting for FH status, girls had 0.11 mmol/L higher TC and 0.10 mmol/L higher LDL-C (both p < 0.05).</p><p><strong>Conclusion: </strong>Prepubertal girls have modestly higher TC and LDL-C than boys, a difference not observed in prepubertal FH-positive children, suggesting that the presence of a pathogenic FH variant may override innate physiological differences in lipid metabolism. These findings support universal early cholesterol screening and suggest that sex-specific reference values may improve early cardiovascular risk assessment in prepubertal FH-negative children.</p>","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":" ","pages":"120484"},"PeriodicalIF":5.7,"publicationDate":"2025-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144940632","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}