Atherosclerosis最新文献

{"title":"Efficacy and safety of statins, ezetimibe and statins-ezetimibe therapies for children and adolescents with heterozygous familial hypercholesterolaemia: Systematic review, pairwise and network meta-analyses of randomised controlled trials.","authors":"Alexis Llewellyn, Mark Simmonds, David Marshall, Melissa Harden, Beth Woods, Steve E Humphries, Uma Ramaswami, Lorraine Priestley-Barnham, Mark Fisher, Laila J Tata, Nadeem Qureshi","doi":"10.1016/j.atherosclerosis.2024.118598","DOIUrl":"https://doi.org/10.1016/j.atherosclerosis.2024.118598","url":null,"abstract":"<p><strong>Background and aims: </strong>Statins, ezetimibe and statins-ezetimibe combination therapy are recommended lipid-lowering therapies (LLTs) in children with heterozygous familial hypercholesterolaemia (HeFH). However, their relative effectiveness is not well understood. We aimed to compare the safety and efficacy of these therapies using direct and indirect comparisons.</p><p><strong>Methods: </strong>We conducted systematic review, pairwise and network meta-analyses (NMAs) of randomised-controlled trials (RCTs) of statins, ezetimibe and statins-ezetimibe combination therapy in people <18 years with HeFH. Comprehensive bibliographic searches were conducted in December 2022, and a Medline update in January 2024. NMA models accounted for drug class, statin type and dosage.</p><p><strong>Results: </strong>Thirteen RCTs were included (n = 1649, median age 13 years, follow-up 6 weeks-2 years). All LLTs reduced low-density lipoprotein cholesterol (LDL-C) and total cholesterol; statins led to increases in high-density lipoprotein cholesterol and reductions in triglycerides. Statins reduced LDL-C by 33.61 % against placebo (95 % CI 27.58 to 39.63, I² = 83 %). Adding ezetimibe to statins reduced LDL-C by an additional 15.85 % (95 % CI 11.91 to 19.79). NMAs showed intermediate-dose statins reduced LDL-C by an additional 4.77 % compared with lower-doses statins (95 % CrI -11.22 to 1.05); higher-dose statins and intermediate-dose statins + ezetimibe may be similarly effective and are probably superior to ezetimibe, intermediate-and lower-dose statins. There was no evidence of differences in maturation, safety or tolerability between LLTs and placebo.</p><p><strong>Conclusions: </strong>Statins, ezetimibe and statins-ezetimibe are all effective treatments for children with HeFH, but the magnitude of LDL-C reductions varies and may depend on treatment dosage and combination. No safety or tolerability issues were found. Longer-term safety and effectiveness are uncertain.</p>","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":" ","pages":"118598"},"PeriodicalIF":4.9,"publicationDate":"2024-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142340190","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":"Relationship of proteins and subclinical cardiovascular traits in the population-based LIFE-Adult study","authors":"Tarcyane Garcia ,&nbsp;Agnese Petrera ,&nbsp;Stefanie M. Hauck ,&nbsp;Ronny Baber ,&nbsp;Kerstin Wirkner ,&nbsp;Holger Kirsten ,&nbsp;Janne Pott ,&nbsp;Anke Tönjes ,&nbsp;Sylvia Henger ,&nbsp;Markus Loeffler ,&nbsp;Annette Peters ,&nbsp;Markus Scholz","doi":"10.1016/j.atherosclerosis.2024.118613","DOIUrl":"10.1016/j.atherosclerosis.2024.118613","url":null,"abstract":"<div><h3>Background and aims</h3><div>Understanding molecular processes of the early phase of atherosclerotic cardiovascular disease conditions is of utmost importance for early prediction and intervention measures.</div></div><div><h3>Methods</h3><div>We measured 92 cardiovascular-disease-related proteins (Olink, Cardiovascular III) in 2024 elderly participants of the population-based LIFE-Adult study. We analysed the impact of 27 covariables on these proteins including blood counts, cardiovascular risk factors and life-style-related parameters. We also analysed protein associations with 13 subclinical cardiovascular traits comprising carotid intima media thickness, plaque burden, three modes of Vicorder-based pulse-wave velocities, ankle-brachial index and ECLIA-based N-terminal prohormone of brain natriuretic peptide (NT-proBNP).</div></div><div><h3>Results</h3><div>Estimated glomerular filtration rate, triglycerides and sex where the most relevant covariables explaining more than 1 % variance of 49, 22 and 20 proteins, respectively. A total of 43 proteins were significantly associated with at least one of the analysed subclinical cardiovascular traits. NT-pro-BNP, brachial-ankle pulse-wave velocity (baPWV) and parameters of carotid plaque burden accounted for the largest number of associations. Association overlaps were relatively sparse. Only growth/differentiation factor 15, low density lipoprotein receptor and interleukin-1 receptor type 2 are associated with these three different cardiovascular traits. We confirmed several literature findings and found yet unreported associations for carotid plaque presence (von-Willebrand factor, galectin 4), carotid intima-media thickness (carboxypeptidase A1 andB1), baPWV (cathepsin D) and NT-proBNP (cathepsin Z, low density lipoprotein receptor, neurogenic locus homolog protein 3, trem-like transcript 2). Sex-interaction effects were observed, e.g. for spondin-1 and growth/differentiation factor 15 likely regulated by androgen response elements.</div></div><div><h3>Conclusions</h3><div>We extend the catalogue of proteome biomarkers possibly involved in early stages of cardiovascular disease pathologies providing targets for early risk prediction or intervention strategies.</div></div>","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"398 ","pages":"Article 118613"},"PeriodicalIF":4.9,"publicationDate":"2024-09-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142328118","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":"Lipids, lipoproteins, and apolipoproteins: Associations with cognition and dementia","authors":"Ida Juul Rasmussen ,&nbsp;Jiao Luo ,&nbsp;Ruth Frikke-Schmidt","doi":"10.1016/j.atherosclerosis.2024.118614","DOIUrl":"10.1016/j.atherosclerosis.2024.118614","url":null,"abstract":"<div><div>Due to increasing lifespan and aging populations globally there has been a steep rise in late-life dementia, which is now the second most common cause of death in high-income countries. In general, dementia can be divided into two major groups: Alzheimer's disease (AD) and vascular-related dementia (VD). AD is pathologically characterised by senile plaques containing amyloid-β and neurofibrillary tangles composed of hyperphosphorylated tau, whereas VD is dominated by vascular pathology such as cerebral small vessel disease, major strokes, and white matter lesions. Recently, the importance of vascular components in AD is increasingly recognized and it is estimated that up to 45 % of all dementia cases can be prevented by preventing or treating midlife cardiovascular risk factors such as physical inactivity, diabetes, and hypertension. Even though the brain contains approximately 25 % of the total body cholesterol pool, and several genetic variants related to the lipid metabolism have been identified in genome-wide associations studies of AD, the role of lipids, lipoproteins, and apolipoproteins in dementia risk is less well-known.</div><div>In this review, we go through the current literature on lipids, lipoproteins, and apolipoproteins and risk of dementia. We conclude that the evidence is primarily insufficient or conflicting, possibly due to nonoptimal study designs. The future calls for large, prospective studies of midlife measurements of lipids, lipoproteins, and apolipoproteins and one-sample, individual level data Mendelian randomization studies to overcome survival bias. However, the current literature suggests that it is safe to say that what is good for the heart is good for the brain.</div></div>","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"398 ","pages":"Article 118614"},"PeriodicalIF":4.9,"publicationDate":"2024-09-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142328082","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":"The German Lipoprotein Apheresis Registry-Summary of the eleventh annual report","authors":"V.J.J. Schettler ,&nbsp;N. Selke ,&nbsp;S. Jenke ,&nbsp;T. Zimmermann ,&nbsp;G. Schlieper ,&nbsp;W. Bernhardt ,&nbsp;F. Heigl ,&nbsp;P. Grützmacher ,&nbsp;I. Löhlein ,&nbsp;R. Klingel ,&nbsp;B. Hohenstein ,&nbsp;W. Ramlow ,&nbsp;A. Vogt ,&nbsp;U. Julius ,&nbsp;Scientific Board of GLAR for the German Apheresis Working Group","doi":"10.1016/j.atherosclerosis.2024.118601","DOIUrl":"10.1016/j.atherosclerosis.2024.118601","url":null,"abstract":"<div><h3>Background</h3><div>In 2012, the German Lipoprotein Apheresis Registry (GLAR) was launched. Real-world data on lipoprotein apheresis (LA) treatment are now available for a time period of 11 years. All patients received the maximally tolerated lipid-lowering therapy, which included statins, ezetimibe, bempedoic acid, and either proprotein convertase subtilisin/kexin type 9 (PCSK9) antibodies or antisense therapy.</div></div><div><h3>Methods and Results</h3><div>During the time period from 2012 to 2022, 92 German apheresis centers collected retrospective and prospective observational data of a total of 2,301 patients undergoing regular lipoprotein apheresis (LA) treatment of hypercholesterolemia or/and Lp(a)-hyperlipoproteinemia suffering from progressive atherosclerotic cardiovascular disease (ASCVD), with complete data sets of 1.125 patients, who were the subject of this analysis. More than 61,500 LA sessions are documented in the database. In 2022, all patients treated with LA demonstrated a significant immediate median reduction rate of LDL-C (68.8 %) and Lp(a) (72.9 %). Patient data were analyzed for the incidence rate of major coronary events (MACE) 1 and 2 years before the beginning of LA treatment (y-2 and y-1) and prospectively up to eleven years on LA treatment (y+1 to y+11). During the first two years of LA treatment (y+1 and y+2), a MACE reduction of 73 % was observed and continued to be low during y+3 to y+11, when all LA patients were analyzed. LA patients with only increased Lp(a) levels (Lp(a) ≥ 60 mg/dl (≥120 nmol/l) and an LDL-C &lt; 100 mg/dl (&lt;2.6 mmol/l)) had a higher MACE reduction (85 %; n = 443) in the first two years of LA treatment compared to LA patients with only increased LDL-C-levels (LDL-C ≥ 100 mg/dl (≥2.6 mmol/l); Lp(a) &lt; 60 mg/dl (&lt;120 nmol/l)) (53 %; n = 171). Adverse events of LA remained low (about 5 %) over the eleven years and mainly represented puncture problems (1.0 %). No side effects resulted in termination of LA therapy.</div></div><div><h3>Conclusions</h3><div>The current analysis of GLAR data indicates that regular LA leads to very low incidence rates of cardiovascular events in patients with high LDL-C and/or high Lp(a) levels, progressive ASCVD, and maximally tolerated lipid-lowering medication, including proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibition. Additionally, LA was safe with a low rate of adverse effects over an 11-year period. The number of enrolled patients and the duration of observation establish GLAR as the largest LA registry worldwide.</div></div>","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"398 ","pages":"Article 118601"},"PeriodicalIF":4.9,"publicationDate":"2024-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142328119","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 singular French PCSK9-p.Ser127Arg gain-of-function variant: A significant player in cholesterol levels from a 775-year-old common ancestor","authors":"Yara Azar ,&nbsp;Thomas E. Ludwig ,&nbsp;Hugo Le Bon ,&nbsp;Thea Bismo Strøm ,&nbsp;Olivier Bluteau ,&nbsp;Mathilde Di-Filippo ,&nbsp;Alain Carrié ,&nbsp;Hedi Chtioui ,&nbsp;Sophie Béliard ,&nbsp;Oriane Marmontel ,&nbsp;Annie Fonteille ,&nbsp;Maite Gebhart ,&nbsp;Noël Peretti ,&nbsp;Philippe Moulin ,&nbsp;Jean Ferrières ,&nbsp;Alain Pradignac ,&nbsp;Michel Farnier ,&nbsp;Antonio Gallo ,&nbsp;Cécile Yelnik ,&nbsp;Dirk Blom ,&nbsp;Mathilde Varret","doi":"10.1016/j.atherosclerosis.2024.118596","DOIUrl":"10.1016/j.atherosclerosis.2024.118596","url":null,"abstract":"<div><h3>Background and aims</h3><div>PCSK9 is a key regulator of LDL-cholesterol levels. PCSK9 gain of function variants (GOFVs) cause autosomal dominant hypercholesterolemia (ADH). The first described PCSK9-GOFV, p.Ser127Arg, almost exclusively reported in France, represents 67 % of the PCSK9 French GOFVs due to a founder effect. Few other carriers are reported in South Africa and Norway. This study aims to estimate when the common ancestor lived and to describe a cohort of p.Ser127Arg carriers.</div></div><div><h3>Methods</h3><div>Eight families and 14 p.Ser127Arg carriers were genotyped and phenotyped. Haplotypes were constructed using 11 microsatellites around <em>PCSK9</em> and 6 intragenic single nucleotide polymorphisms (SNPs). To add to the biological analysis, eight additional p.Ser127Arg carriers, 12 carriers of other PCSK9-GOFVs, 93 LDLR loss of function variant (LOFV) carriers and 49 non-carriers subjects were phenotyped.</div></div><div><h3>Results</h3><div>The most common ancestor of p.Ser127Arg was estimated to have lived 775 years ago [95 % CI: 575-1075]. French Protestants exiled after the revocation of the Edict of Nantes in 1685 AD likely brought the variant to South Africa and Norway. As expected for ADH subjects, carriers of LDLR-LOFV, the p.Ser127Arg, or other PCSK9-GOFVs showed significantly higher LDL-C levels than that of the non-carriers. Interestingly, LDL-C levels are higher for LDLR-LOFVs and for the reduced secreted p.Ser127Arg than for secreted PCSK9-GOFVs, suggesting a greater effect of the p.Ser127Arg. Conversely, HDL-C was significantly lower for LDLR-LOFV and p.Ser127Arg carriers.</div></div><div><h3>Conclusions</h3><div>This first report from a large cohort of PCSK9-p.Ser127Arg carriers provides observations suggesting a stronger hypercholesterolemic potential of the mutated pro-PCSK9 compared with the secreted mature protein. This work also provides additional data to support the association between PCSK9 and HDL metabolism, and molecular evidence that this variant appeared in France around 1248 <span>AD (Graphical Abstract = Fig. 1)</span>.</div></div>","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"399 ","pages":"Article 118596"},"PeriodicalIF":4.9,"publicationDate":"2024-09-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142578096","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":"In Memoriam: Akira Endo (1933-2024)","authors":"Alberico L. Catapano","doi":"10.1016/j.atherosclerosis.2024.118545","DOIUrl":"10.1016/j.atherosclerosis.2024.118545","url":null,"abstract":"","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"397 ","pages":"Article 118545"},"PeriodicalIF":4.9,"publicationDate":"2024-09-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0021915024011134/pdfft?md5=f5a42ca44558e0d4b41ad004f3a95fa8&pid=1-s2.0-S0021915024011134-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142228668","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":"The association between trimethylamine N-oxide levels and coronary microvascular dysfunction and prognosis in patients with ST-elevation myocardial infarction","authors":"Ali Aldujeli ,&nbsp;Tsung-Ying Tsai ,&nbsp;Ayman Haq ,&nbsp;Vacis Tatarunas ,&nbsp;Scot Garg ,&nbsp;Diarmaid Hughes ,&nbsp;Ieva Ciapiene ,&nbsp;Ramunas Unikas ,&nbsp;Faisal Sharif ,&nbsp;Vaiva Lesauskaite ,&nbsp;Yoshinobu Onuma ,&nbsp;Patrick W. Serruys","doi":"10.1016/j.atherosclerosis.2024.118597","DOIUrl":"10.1016/j.atherosclerosis.2024.118597","url":null,"abstract":"<div><h3>Background and aims</h3><div>Coronary microvascular dysfunction (CMD) is common after ST-elevation myocardial infarction (STEMI), leading to adverse clinical outcomes. However, its diagnosis remains difficult, and mechanisms elusive. This study explores the role of Trimethylamine N-oxide (TMAO), a gut microbiota metabolite, as a potential biomarker for diagnosing CMD in STEMI patients.</div></div><div><h3>Methods</h3><div>This prospective, observational study enrolled 210 STEMI patients with multivessel coronary artery disease who underwent primary percutaneous coronary intervention (PCI). TMAO levels were measured at baseline, 3 months, and 12 months post-PCI, whilst coronary physiology was assessed at 3 months. The primary endpoint was the incidence of CMD at 3 months, with the secondary endpoint being major adverse cardiovascular and cerebrovascular events (MACCE) at 12 months. An additional 59 consecutive patients were enrolled for validation.</div></div><div><h3>Results</h3><div>TMAO levels varied from baseline to 3 months, then stabilised. The areas under the ROC curve for baseline TMAO and TMAO at 3-month were 0.55 (95 % CI 0.46–0.64; <em>p</em> = 0.426), and 0.80 (95 % CI 0.73–0.87; <em>p</em> &lt; 0.001), respectively. The optimal cut-off for TMAO at 3-month to diagnose CMD was 3.91, with similar sensitivity and specificity in the derivation and validation cohort. The incidence of MACCE was higher in patients with TMAO≥3.91 (41.4 % vs 10.7 %; <em>p</em> &lt; 0.001). The addition of 3-month TMAO improved the diagnostic performance of traditional risk factors.</div></div><div><h3>Conclusion</h3><div>TMAO is a robust biomarker for CMD and is significantly associated with the incidence of MACCE. TMAO has the potential in guiding clinical decision-making and suggests an interplay between gut microbiota and CMD.</div></div>","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"398 ","pages":"Article 118597"},"PeriodicalIF":4.9,"publicationDate":"2024-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142311560","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":"Arterial inflammation on [18F]FDG PET/CT in melanoma patients treated with and without immune checkpoint inhibitors: CHECK-FLAME I","authors":"Elissa A.S. Polomski ,&nbsp;Ellen W. Kapiteijn ,&nbsp;Julius C. Heemelaar ,&nbsp;Anne V. van der Kolk ,&nbsp;Timo M. Kalisvaart ,&nbsp;Alina van de Burgt ,&nbsp;Petra Dibbets-Schneider ,&nbsp;Floris H.P. van Velden ,&nbsp;Tom T.P. Seijkens ,&nbsp;J. Lauran Stöger ,&nbsp;J. Wouter Jukema ,&nbsp;Lioe-Fee de Geus-Oei ,&nbsp;M. Louisa Antoni","doi":"10.1016/j.atherosclerosis.2024.118595","DOIUrl":"10.1016/j.atherosclerosis.2024.118595","url":null,"abstract":"<div><h3>Background and aims</h3><p>Immune checkpoint inhibitors (ICIs) revolutionized cancer treatment. However, ICIs may increase the immune response to non-tumor cells, possibly resulting in increased arterial inflammation, raising the risk of atherosclerotic events. Nevertheless, malignancies may induce a pro-inflammatory state and the association between ICIs and arterial inflammation remains to be clarified. This study aims to assess differences in increase in arterial inflammation between patients with advanced melanoma treated with ICIs compared to a control group without ICIs.</p></div><div><h3>Methods</h3><p>Patients with advanced melanoma who underwent [¹⁸F]FDG PET/CT scans at baseline, 6 months (T1) and 18 months (T2) were included in this retrospective observational study. Arterial inflammation was evaluated in eight segments by calculating the target-to-background ratio (TBR). The primary study outcome was the difference in increase in mean TBR_max between patients treated with and without ICIs.</p></div><div><h3>Results</h3><p>We included 132 patients of whom 72.7 % were treated with ICIs. After exclusion for the use of anti-inflammatory medication, patients treated with ICIs showed a significant increase in mean TBR_max between baseline and T1 from 1.29 ± 0.12 to 1.33 ± 0.13 (<em>p =</em> 0.017), while in the control group, no change in mean TBR_max (1.30 ± 0.12 to 1.28 ± 0.10, <em>p =</em> 0.22) was observed (<em>p =</em> 0.027). During longer follow-up, mean TBR_max remained stable in both groups. Arterial inflammation increased significantly after ICI therapy in patients without active inflammation (<em>p</em> &lt; 0.001) and in patients without calcifications (<em>p =</em> 0.013).</p></div><div><h3>Conclusions</h3><p>A significant increase in arterial inflammation as measured on [¹⁸F]FDG PET/CT was observed in patients with advanced melanoma treated with ICIs only in the first six months after initiation of therapy, whereas no changes were observed in the control group. Moreover, arterial inflammation was mainly increased in patients without pre-existing inflammatory activity and with non-calcified lesions.</p></div>","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"398 ","pages":"Article 118595"},"PeriodicalIF":4.9,"publicationDate":"2024-09-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0021915024011675/pdfft?md5=21ad258d1059bd9674acf07956182932&pid=1-s2.0-S0021915024011675-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142272941","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":"Is colchicine on its way to a place in the polypill for cardiovascular prevention?","authors":"Fernando Botto,&nbsp;Sebastián Garcia-Zamora","doi":"10.1016/j.atherosclerosis.2024.118594","DOIUrl":"10.1016/j.atherosclerosis.2024.118594","url":null,"abstract":"","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"398 ","pages":"Article 118594"},"PeriodicalIF":4.9,"publicationDate":"2024-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142269958","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":"Silencing ARL11 relieved atherosclerotic inflammation and lipid deposition via retraining JAK2/STAT1 pathway","authors":"Yanhua Zhen ,&nbsp;Jiaqi Yang ,&nbsp;Ji Song ,&nbsp;Zeyu Xing ,&nbsp;Jiahe Zheng","doi":"10.1016/j.atherosclerosis.2024.118564","DOIUrl":"10.1016/j.atherosclerosis.2024.118564","url":null,"abstract":"<div><h3>Background and aims</h3><div>Atherosclerosis (AS), an arterial vasculature disease, is characterized by abnormal lipid accumulation and inflammatory response. ADP ribosylation factor like GTPase 11 (ARL11) is linked to multifarious processes in cells. This study aims to clarify the underlying mechanism of ARL11 in AS.</div></div><div><h3>Methods</h3><div><em>ApoE</em>^{<em>−/−</em>} mice fed with high-fat diet were used as mouse model of AS. Gene expression in AS was determined by mRNA-sequencing. ARL11 expression was detected by real-time PCR, Western blot and immunofluorescence. M1 polarization of macrophages was indicated by TNF-α and IL-6 levels as detected with ELISA, and iNOS expression determined by real-time PCR and Western blot. The role of ARL11 during AS was explored through loss-of-function analysis.</div></div><div><h3>Results</h3><div>There were 1301 upregulated and 1110 downregulated genes during AS. These differentially expressed genes (DEGs) were mainly enriched in pathways and terms which are involved in inflammation. Moreover, <em>Arl11</em> was highly expressed in AS models. Downregulation of <em>Arl11</em> decreased lipid deposition and atherosclerotic plaques in the aortas of AS mice, and declined inflammatory cytokines and M1 polarization of macrophages induced by IFN-γ. Furthermore, ARL11 interacted with JAK2 and p-JAK2 and modulated their degradation, thus inhibiting the activation of JAK2/STAT1 pathway.</div></div><div><h3>Conclusions</h3><div>ARL11 promoted the development of AS via interacting with JAK2 and activating JAK2/STAT1 pathway. Thus, silencing ARL11 may prevent the process of AS and be a novel way to treat AS.</div></div>","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"398 ","pages":"Article 118564"},"PeriodicalIF":4.9,"publicationDate":"2024-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142307013","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}