Atherosclerosis最新文献

{"title":"Corrigendum to “Familial chylomicronemia syndrome and treatments to target hepatic APOC3 mRNA” [Atherosclerosis (2025) 403 119114]","authors":"Eliot A. Brinton , Robert H. Eckel , Daniel Gaudet , Christie M. Ballantyne , Brenda F. Baker , Henry N. Ginsberg , Joseph L. Witztum","doi":"10.1016/j.atherosclerosis.2025.119210","DOIUrl":"10.1016/j.atherosclerosis.2025.119210","url":null,"abstract":"","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"405 ","pages":"Article 119210"},"PeriodicalIF":4.9,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143891739","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":"Immune-related biochemical markers and 20-year incidence of atherosclerotic cardiovascular disease: the ATTICA study (2002–2022)","authors":"Sofia-Panagiota Giannakopoulou ,&nbsp;Christina Chrysohoou ,&nbsp;Smaragdi Antonopoulou ,&nbsp;Fotios Barkas ,&nbsp;Nikos Vlachogiannis ,&nbsp;Evrydiki Kravvariti ,&nbsp;Evangelos Liberopoulos ,&nbsp;Christos Pitsavos ,&nbsp;Costas Tsioufis ,&nbsp;Demosthenes Panagiotakos ,&nbsp;Petros P. Sfikakis","doi":"10.1016/j.atherosclerosis.2025.119212","DOIUrl":"10.1016/j.atherosclerosis.2025.119212","url":null,"abstract":"<div><h3>Background and aims</h3><div>Inflammation has been associated with increased atherosclerotic cardiovascular disease (ASCVD) risk. We evaluated immune-related biomarkers regarding their ability, individually and as a composite score, to predict 20-year ASCVD incidence in an apparently healthy adult population.</div></div><div><h3>Methods</h3><div>A cohort of 1270 adults, who were free of ASCVD at baseline, with a 20-year follow-up from the prospective ATTICA study, were included in this analysis. Immune-related biochemical markers independently predictive of 20-year ASCVD risk were identified, and an aggregate biomarker score was developed. The incremental predictive value of this score beyond the SCORE2 was assessed using area under the receiver operating characteristic curve (AUC), net reclassification improvement (NRI), and integrated discrimination improvement (IDI).</div></div><div><h3>Results</h3><div>Three immune-related biomarkers -interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α) and fibrinogen-showed the best predictive ability of 20-year ASCVD risk and were subsequently integrated into an aggregate biomarker score (ImmActScore), exhibiting a range from 0 (6 % absolute risk) to 4 (63 % absolute risk). Individual ImmActScore was independently associated with 20-year ASCVD risk (multi-adjusted HR per 1-unit:1.24, 95 %CI:1.05–1.46, <em>p</em> = 0.011). The 38.5 % of the 20-year incident ASCVD could be attributed to ImmActScores of ≥1. Integrating ImmActScore into the SCORE2 model yielded a continuous NRI of 0.603 and a categorical NRI of 18.4 % in the 40–50 year age group.</div></div><div><h3>Conclusions</h3><div>Assessing immune-related pathways may offer additional potential for long-term ASCVD risk stratification. A combined measure of IL-6, TNF-α and fibrinogen levels was associated with ASCVD events over a 20-year period. Further validation in independent cohorts is warranted.</div></div>","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"405 ","pages":"Article 119212"},"PeriodicalIF":4.9,"publicationDate":"2025-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143882788","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":"Lipid metabolism in women: A review","authors":"Julie A.E. van Oortmerssen ,&nbsp;Janneke W.C.M. Mulder ,&nbsp;Maryam Kavousi ,&nbsp;Jeanine E. Roeters van Lennep","doi":"10.1016/j.atherosclerosis.2025.119213","DOIUrl":"10.1016/j.atherosclerosis.2025.119213","url":null,"abstract":"<div><div>The menopausal transition, defined by the cessation of menstruation due to declining ovarian follicular function, results in a marked decrease in endogenous estrogen levels. This phase is associated with significant metabolic changes and a shift towards a more atherogenic lipid profile. Specifically, there are increases in total cholesterol, low-density lipoprotein cholesterol, and triglycerides and unfavorable alterations in high-density lipoprotein cholesterol and lipoprotein(a) levels. These lipid changes, which contribute to an increased risk of atherosclerotic cardiovascular disease, are influenced by diminished estrogen levels and chronological aging. However, the specific mechanisms driving this increased risk are not fully understood. A thorough understanding of these lipid profile alterations is important for developing strategies to reduce cardiovascular disease risk in women. This review provides an overview of how lipid metabolism is affected during the menopausal transition and the resulting implications for cardiovascular risk.</div></div>","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"405 ","pages":"Article 119213"},"PeriodicalIF":4.9,"publicationDate":"2025-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143882787","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":"Frequency of residual combined dyslipidemia and hypertriglyceridemia in patients with coronary heart disease in 13 countries across 6 WHO Regions: Results from INTERASPIRE","authors":"Raul D. Santos ,&nbsp;Kausik K. Ray ,&nbsp;Dirk De Bacquer ,&nbsp;Catriona Jennings ,&nbsp;Kornelia Kotseva ,&nbsp;Lars Rydén ,&nbsp;Gregory Y.H. Lip ,&nbsp;Iris Erlund ,&nbsp;Sandra Ganly ,&nbsp;Terhi Vihervaara ,&nbsp;Agnieszka Adamska ,&nbsp;Ana Abreu ,&nbsp;Wael Almahmeed ,&nbsp;Ade Meidian Ambari ,&nbsp;Junbo Ge ,&nbsp;Hosam Hasan-Ali ,&nbsp;Yong Huo ,&nbsp;Piotr Jankowski ,&nbsp;Rodney M. Jimenez ,&nbsp;Yong Li ,&nbsp;Peter Libby","doi":"10.1016/j.atherosclerosis.2025.119215","DOIUrl":"10.1016/j.atherosclerosis.2025.119215","url":null,"abstract":"<div><h3>Background and aims</h3><div>Hypertriglyceridemia (HTG) is independently associated with risk of atherosclerotic events, even when LDL-cholesterol levels appear controlled. This INTERASPIRE study determined the frequency of HTG and residual combined dyslipidemia and their related factors in patients with coronary heart disease (CHD) from 13 countries across six World Health Organization (WHO) regions.</div></div><div><h3>Methods</h3><div>Participants with CHD underwent a standardized study interview and examination, including a centralized analysis of fasting blood samples. Elevated triglyceride (TG) and LDL-cholesterol were defined as ≥ 1.7 mmol/L and 1.8 mmol/L, respectively. Elevation in both was considered combined dyslipidemia.</div></div><div><h3>Results</h3><div>Lipid profiles were available for 4069 patients. The mean age was 60.1 years (21.1 % women, 12.6 % smokers, 24 % obesity by body mass index [BMI], 61 % hypertension, and 44 % self-reported diabetes). Participants were evaluated 1.05 (0.76–1.45) years after their index CHD hospitalization. Overall, 12.7 % used no lipid-lowering therapies (LLT), 50.0 % used high-dose statins, and 11.8 % used combination therapies. Specific TG-lowering therapies were used by 2.3 %. One-third of patients had HTG, and 24.6 % had combined dyslipidemia. HTG was seen in all countries, but median TG values varied, with higher values among those not using LLT. HTG was independently associated with female sex, smoking, BMI, blood pressure, and LDL-cholesterol. HTG was inversely associated with HDL-cholesterol.</div></div><div><h3>Conclusions</h3><div>HTG and residual combined dyslipidemia are common, although with wide variability between countries. A healthier lifestyle, weight reduction, greater use of combination therapy, and evidence-based TG-lowering treatments are necessary to reduce the risks of HTG and combined dyslipidemia.</div></div>","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"405 ","pages":"Article 119215"},"PeriodicalIF":4.9,"publicationDate":"2025-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143890534","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":"Low functional capacity in peripheral artery disease is associated with increased platelet activity and cardiovascular events","authors":"Sean P. Heffron ,&nbsp;Matt Muller ,&nbsp;Yuhe Xia ,&nbsp;Elliot Luttrell-Williams ,&nbsp;Caron B. Rockman ,&nbsp;Jonathan D. Newman ,&nbsp;Crystalann Rodriguez ,&nbsp;Tessa J. Barrett ,&nbsp;Jeffrey S. Berger","doi":"10.1016/j.atherosclerosis.2025.119200","DOIUrl":"10.1016/j.atherosclerosis.2025.119200","url":null,"abstract":"<div><h3>Background and aims</h3><div>Low functional capacity is an independent risk factor for cardiovascular (CV) events. Regular physical activity may reduce CV risk through suppression of inflammation and reduced platelet activity. We aimed to investigate the association of functional capacity quantified by the validated Duke Activity Status Index (DASI) with platelet activity and incident major adverse CV and limb events (MACLE) in individuals with peripheral artery disease (PAD) undergoing lower extremity revascularization (LER).</div></div><div><h3>Methods</h3><div>Light transmission aggregometry and platelet RNAseq were performed on specimens isolated from men and women prior to LER. Functional capacity was assessed using DASI. Prospective follow-up occurred at 1, 6, 12, and every 6 months following the LER. Subjects were separated into tertiles of DASI scores and incidence rates for MACLE were calculated using log-rank tests. Mediation analysis using linear regression fit with least squares was performed to test whether DASI exerted its effect on MACLE via platelet aggregation.</div></div><div><h3>Results</h3><div>281 patients completed the DASI questionnaire with scores ranging from 0.0 to 50.2 (bottom tertile: 0.0–9.95). Mean age was 74.4 ± 10.9 years and 32.4 % were female.</div><div>During a median follow-up of 19 months, 163 (58.0 %) participants experienced a MACLE. After correction for demographics and CV risk factors, individuals in the lowest DASI tertile experienced significantly more MACLE than participants in other tertiles. The association between DASI and MACLE was consistent across multiple subgroups stratified by age, sex, body mass index, antiplatelet therapy, and clinical comorbidities. Mediation analyses suggested higher platelet aggregation to epinephrine in the bottom DASI tertile mediated 24.7 % [5.0 %, 103 %] of increased MACLE risk. Platelet mRNA demonstrated upregulation of inflammation pathways in the most sedentary individuals (lowest DASI tertile).</div></div><div><h3>Conclusions</h3><div>Patients with PAD and low functional capacity have increased platelet activity and high incidence of MACLE. Our data suggest that elevated platelet aggregation mediates one-quarter of the MACLE risk in persons with low functional capacity undergoing LER. Our findings support a potential platelet-mediated mechanism for improved CV outcomes associated with regular physical activity.</div></div>","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"405 ","pages":"Article 119200"},"PeriodicalIF":4.9,"publicationDate":"2025-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143891738","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":"Corrigendum to EAS Abstracts 2024 [Atherosclerosis (2024) Article number; 117943, 118076, 118078]","authors":"","doi":"10.1016/j.atherosclerosis.2025.119182","DOIUrl":"10.1016/j.atherosclerosis.2025.119182","url":null,"abstract":"","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"404 ","pages":"Article 119182"},"PeriodicalIF":4.9,"publicationDate":"2025-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143791071","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Loss of ADAMTS5 promotes vascular calcification via versican/integrin β1/FAK signal","authors":"Zhenyu Zhu ,&nbsp;Hao Liu ,&nbsp;Liyun Feng ,&nbsp;Lihe Lu ,&nbsp;Jiahui Zhu ,&nbsp;Qingchun Liang ,&nbsp;Zirong Lan ,&nbsp;Yuanzhi Ye ,&nbsp;Siyi Wang ,&nbsp;An Chen ,&nbsp;Jianyun Yan","doi":"10.1016/j.atherosclerosis.2025.119190","DOIUrl":"10.1016/j.atherosclerosis.2025.119190","url":null,"abstract":"<div><h3>Introduction</h3><div>Extracellular matrix (ECM) proteases have been closely linked to the pathogenesis of vascular calcification. A disintegrin and metalloprotease with thrombospondin motifs-5 (ADAMTS5) is an ECM-degrading enzyme involved in ECM remodeling. Versican, a critical ECM component in the arteries, can be proteolytically cleaved by ADAMTS5 and activates integrin β1. However, whether ADAMTS5 is involved in the regulation of the pathogenesis of vascular calcification remains unclear. This study investigates the regulatory role of ADAMTS5 in vascular calcification and its mechanistic link to versican-integrin β1/FAK signaling.</div></div><div><h3>Methods and results</h3><div>Western blot, immunofluorescence, and immunohistochemistry analysis revealed that <em>ADAMTS5</em> expression was significantly downregulated in rat and human vascular smooth muscle cells (VSMCs), as well as in rat and human arteries during vascular calcification. In addition, both pharmacological inhibition of ADAMTS5 and knockdown of <em>ADAMTS5</em> by siRNA significantly aggravated mineral deposition in rat and human VSMCs under osteogenic conditions. Moreover, adenovirus-mediated <em>ADAMTS5</em> overexpression markedly attenuated calcification of VSMCs and aortic calcification in rats with chronic kidney disease. Furthermore, inhibition of ADAMTS5 promoted aortic calcification in VitD₃-overloaded mice. Mechanistically, overexpression of <em>ADAMTS5</em> significantly reduced versican protein levels, and inhibited integrin β1 and FAK phosphorylation in rat VSMCs, but increased versikine protein levels. Moreover, either knockdown of versican or pharmacological inhibition of FAK phosphorylation repressed VSMC calcification mediated by loss of ADAMTS5.</div></div><div><h3>Conclusions</h3><div>We have demonstrated for the first time that ADAMTS5 deficiency promotes versican accumulation and activates integrin β1/FAK signaling. These findings suggest ADAMTS5 as a potential therapeutic target for vascular calcification.</div></div>","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"404 ","pages":"Article 119190"},"PeriodicalIF":4.9,"publicationDate":"2025-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143817243","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":"Why has the “Lp(a) receptor” proven so elusive?","authors":"Gilles C. Lambert ,&nbsp;Michael B. Boffa","doi":"10.1016/j.atherosclerosis.2025.119189","DOIUrl":"10.1016/j.atherosclerosis.2025.119189","url":null,"abstract":"","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"404 ","pages":"Article 119189"},"PeriodicalIF":4.9,"publicationDate":"2025-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143817242","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 determined increase in apolipoprotein C-III (APOC3 gain-of-function) delays very low-density lipoprotein clearance in humans","authors":"C.J. Packard ,&nbsp;M.R. Taskinen ,&nbsp;E. Björnson ,&nbsp;N. Matikainen ,&nbsp;S. Söderlund ,&nbsp;L. Andersson ,&nbsp;M. Adiels ,&nbsp;J. Borén","doi":"10.1016/j.atherosclerosis.2025.119166","DOIUrl":"10.1016/j.atherosclerosis.2025.119166","url":null,"abstract":"<div><h3>Aim</h3><div>Apolipoprotein C-III (apoC-III) is an important regulator of triglyceride (TG) metabolism and a target for intervention. The present study examined the effects of gain-of-function (GOF) variants in <em>APOC3</em> on apolipoprotein B kinetics to understand further how changes in the synthesis of this apolipoprotein impact triglyceride-rich lipoprotein (TRL) metabolism.</div></div><div><h3>Methods</h3><div>Two groups of subjects were recruited by population screening, 9 carriers of known <em>APOC3</em> GOF variants and 9 age-, sex- and BMI-matched non-carriers. The kinetics of TRL were determined using stable isotope tracers of apoprotein and triglyceride metabolism in a non-steady-state protocol involving administration of a fat-rich meal.</div></div><div><h3>Results</h3><div><em>APOC3</em> GOF carriers had 47 % higher plasma apoC-III levels compared to non-carriers (P = 0.022) and higher production rates for the apolipoprotein. Post-prandial response (total area-under-curve) for plasma TG was 108 % greater in GOF carriers compared to non-carriers (P = 0.002) due specifically to higher levels of VLDL₁. In contrast, no difference was seen in the chylomicron apoB48 response. Comparison of TRL kinetics between groups showed that <em>APOC3</em> GOF carriers had lower fractional clearance rates for VLDL₁-apoB100 and VLDL₁-apoB48-containing particles (P &lt; 0.02), but no difference in VLDL₁-apoB100 or chylomicron apoB48 production rates. Both the rate of VLDL lipolysis and the rate of clearance of VLDL particles from the circulation were lower in <em>APOC3</em> GOF carriers than in non-carriers. In contrast, chylomicron apoB clearance rates did not differ between <em>APOC3</em> GOF carriers and non-carriers.</div></div><div><h3>Conclusion</h3><div><em>APOC3</em> GOF carriers showed specific alterations in TRL metabolism (compared to matched non-carriers), namely slower lipolysis and delayed clearance of VLDL₁-sized particles, but no difference in chylomicron metabolism. Our findings suggest that intervention to reduce apoC-III production can be modelled as a reduction in TRL, particularly VLDL particle levels, without deleterious effects on fat absorption or hepatic VLDL production.</div></div>","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"404 ","pages":"Article 119166"},"PeriodicalIF":4.9,"publicationDate":"2025-04-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143799716","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Reprogramming human macrophages in symptomatic carotid stenosis: Stabilization of atherosclerotic carotid plaques","authors":"Klaudia Kocsy ,&nbsp;Sumeet Deshmukh ,&nbsp;Shah Nawaz ,&nbsp;Ali N. Ali ,&nbsp;Sheharyar Baig ,&nbsp;Joyce S. Balami ,&nbsp;Arshad Majid ,&nbsp;Endre Kiss-Toth ,&nbsp;Sheila Francis ,&nbsp;Jessica Redgrave","doi":"10.1016/j.atherosclerosis.2025.119180","DOIUrl":"10.1016/j.atherosclerosis.2025.119180","url":null,"abstract":"<div><h3>Background and Aims</h3><div>Inflammation is a precursor to atherosclerotic plaque destabilisation, leading to ischaemic events like stroke. Since macrophage phenotypes can be influenced by their microenvironment, we aimed to stabilise plaques and reduce the risk of recurrent ischaemic events using clinically relevant anti-inflammatory agents.</div></div><div><h3>Methods</h3><div>Thirteen carotid plaques from stroke/Transient Ischaemic Attack (TIA) patients undergoing carotid endarterectomy were analysed using immunofluorescence stain to identify macrophage markers (CD68, CD86, MRC1). An <em>in vitro</em> model of human blood-derived macrophages was used to evaluate the effects of statins and glucocorticoids on macrophage-specific markers using RT-qPCR, Western Blot, and immunofluorescence staining. The physiological effects of dexamethasone on macrophages and human carotid plaques were further studied <em>ex vivo</em>.</div></div><div><h3>Results</h3><div>The macrophage population (CD68⁺) in the carotid plaques was dominated by “double-positive” (CD86+MRC1+) macrophages (67.8 %), followed by “M1-like” (CD86+MRC1-) (16.5 %), “M2-like” (CD86-MRC1+) (8.7 %) and “double-negative” (CD86-MRC1-) (7.0 %) macrophages. M1-like macrophages were more prevalent in unstable plaque sections than stable ones (p = 0.0022). Exposure to dexamethasone increased macrophage <em>MRC1</em> gene expression <em>in vitro</em> and <em>ex vivo</em>. It also reduced the expression of the Oxidised Low-Density Lipoprotein Receptor 1 (<em>OLR1</em>) gene and protein, leading to reduced oxLDL uptake in foam cell assays.</div></div><div><h3>Conclusions</h3><div>Clinically relevant concentrations of glucocorticoids may shift human macrophages to a less inflammatory state, thus reducing their ability for oxidised LDL uptake. In contrast, this anti-inflammatory mechanism was not observed in response to statins. These findings suggest that glucocorticoids could help prevent ischemic events in patients with advanced atherosclerosis.</div></div>","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"404 ","pages":"Article 119180"},"PeriodicalIF":4.9,"publicationDate":"2025-04-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143829127","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}