Atherosclerosis最新文献

英文中文

CCN4 (WISP-1) reduces apoptosis and atherosclerotic plaque burden in an ApoE mouse model CCN4 (WISP-1) 在载脂蛋白E小鼠模型中减少细胞凋亡和动脉粥样硬化斑块负担

IF 4.9 2区医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS

Atherosclerosis

Pub Date : 2024-08-26 DOI: 10.1016/j.atherosclerosis.2024.118570

Background and aims

CCN4/WISP-1 regulates various cell behaviours that contribute to atherosclerosis progression, including cell adhesion, migration, proliferation and survival. We therefore hypothesised that CCN4 regulates the development and progression of atherosclerotic plaques.

Methods

We used a high fat fed ApoE^−/− mouse model to study atherosclerotic plaque progression in the brachiocephalic artery and aortic root. In protocol 1, male ApoE^−/− mice with established plaques were given a CCN4 helper-dependent adenovirus to see the effect of treatment with CCN4, while in protocol 2 male CCN4^−/− ApoE^−/− were compared to CCN4^+/+ApoE^−/− mice to assess the effect of CCN4 deletion on plaque progression.

Results

CCN4 overexpression resulted in reduced occlusion of the brachiocephalic artery with less apoptosis, fewer macrophages, and attenuated lipid core size. The amount of plaque found on the aortic root was also reduced. CCN4 deficiency resulted in increased apoptosis and occlusion of the brachiocephalic artery as well as increased plaque in the aortic root. Additionally, in vitro cells from CCN4^−/− ApoE^−/− mice had higher apoptotic levels. CCN4 deficiency did not significantly affect blood cholesterol levels or circulating myeloid cell populations.

Conclusions

We conclude that in an atherosclerosis model the most important action of CCN4 is the effect on cell apoptosis. CCN4 provides pro-survival signals and leads to reduced cell death, lower macrophage number, smaller lipid core size and reduced atherosclerotic plaque burden. As such, the pro-survival effect of CCN4 is worthy of further investigation, in a bid to find a therapeutic for atherosclerosis.

背景和目的CCN4/WISP-1调节导致动脉粥样硬化进展的各种细胞行为，包括细胞粘附、迁移、增殖和存活。因此，我们推测 CCN4 可调控动脉粥样硬化斑块的形成和进展。方法我们使用高脂喂养的载脂蛋白E-/-小鼠模型来研究肱脑动脉和主动脉根部动脉粥样硬化斑块的进展。在方案1中，给已形成斑块的雄性载脂蛋白E-/-小鼠注射CCN4辅助依赖性腺病毒，以观察CCN4治疗的效果；在方案2中，将雄性CCN4-/-载脂蛋白E-/-小鼠与CCN4+/+载脂蛋白E-/-小鼠进行比较，以评估CCN4缺失对斑块进展的影响。结果CCN4过表达导致肱脑动脉闭塞减少，细胞凋亡减少，巨噬细胞减少，脂质核心大小减小。主动脉根部发现的斑块数量也有所减少。缺乏 CCN4 会导致凋亡增加、肱动脉闭塞以及主动脉根部斑块增加。此外，CCN4-/-载脂蛋白E-/-小鼠的体外细胞凋亡水平更高。结论我们得出结论，在动脉粥样硬化模型中，CCN4最重要的作用是影响细胞凋亡。CCN4提供了促生存信号，导致细胞死亡减少、巨噬细胞数量降低、脂质核心体积缩小以及动脉粥样硬化斑块负担减轻。因此，CCN4的促生存作用值得进一步研究，以找到治疗动脉粥样硬化的方法。

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引用次数: 0

Genetic evidence for lifestyle and cardiometabolic factors on the risk of aortic aneurysms: A comprehensive Mendelian randomization study 生活方式和心脏代谢因素对主动脉瘤风险的遗传学证据：孟德尔随机综合研究

IF 4.9 2区医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS

Atherosclerosis

Pub Date : 2024-08-24 DOI: 10.1016/j.atherosclerosis.2024.118572

Background and aims

Aortic aneurysm (AAs) is a chronic and severe aortic disease, which is extremely life-threatening due to its delayed diagnosis and a high risk of rupture. In current studies, the association between lifestyle and metabolic factors remains controversial given the complexity of pathogenesis and progression in AAs. Consequently, more reliable and robust evidence should be provided.

Methods

Genome-wide association studies summary statistics were obtained for 25 factors (6 lifestyle factors and 19 cardiometabolic factors) and AAs. Univariable Mendelian randomization (UVMR) and multivariable MR (MVMR) were used to estimate the causal effect of these factors on AAs. Meanwhile, mediation analysis was applied to assess the mediated effect of lifestyle on the association of cardiometabolic factors with AAs.

Results

Several factors were associated with AA risk, among which triglyceride (TG) (OR = 1.32, 95 % CI = [1.18–1.47], p < 0.001) and high-density lipoprotein cholesterol (HDL-C) (OR = 0.70, 95 % CI = [0.61–0.82], p < 0.001) remain consistently associated with AA risk, with an idependent effect on AAs after adjusting for body mass index (BMI). In addition, TG mediated 15.6 % of BMI effects and 3.7 % of smoking effects on AAs, and HDL-C mediated 5.3 % of the effects of cigarette smoking on AAs.

Conclusions

TG and HDL-C may be the most reliable factors in the risk of AAs. More scientific management of lifestyle and regular monitoring for cardiometabolic traits may serve as a new and effective direction for the prevention and control of the occurrence of AAs.

背景和目的主动脉瘤（AAs）是一种慢性、严重的主动脉疾病，由于诊断不及时和破裂风险高，极易危及生命。在目前的研究中，生活方式和代谢因素之间的关联仍存在争议，因为 AAs 的发病机制和进展十分复杂。方法对 25 个因素（6 个生活方式因素和 19 个心脏代谢因素）和 AAs 进行了全基因组关联研究，并获得了汇总统计数据。采用单变量孟德尔随机化（UVMR）和多变量 MR（MVMR）来估计这些因素对 AAs 的因果效应。结果几个因素与 AA 风险相关，其中甘油三酯（TG）（OR = 1.32，95 % CI = [1.18-1.47]，p <0.001）和高密度脂蛋白胆固醇（HDL-C）（OR = 0.70，95 % CI = [0.61-0.82]，p <0.001）仍与 AA 风险持续相关，在调整体重指数（BMI）后，对 AA 的影响与之相同。此外，总胆固醇介导了体重指数对 AAs 15.6% 的影响和吸烟对 AAs 3.7% 的影响，而高密度脂蛋白胆固醇介导了吸烟对 AAs 5.3% 的影响。更科学的生活方式管理和定期监测心血管代谢特征可能是预防和控制 AAs 发生的一个新的有效方向。

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引用次数: 0

Phospholipid-derived lysophospholipids in (patho)physiology. 磷脂衍生的溶血磷脂在（病理）生理学中的作用。

IF 4.9 2区医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS

Atherosclerosis

Pub Date : 2024-08-23 DOI: 10.1016/j.atherosclerosis.2024.118569

Patricia Prabutzki, Jürgen Schiller, Kathrin M Engel

Phospholipids (PL) are major components of cellular membranes and changes in PL metabolism have been associated with the pathogenesis of numerous diseases. Lysophosphatidylcholine (LPC) in particular, is a comparably abundant component of oxidatively damaged tissues. LPC originates from the cleavage of phosphatidylcholine (PC) by phospholipase A₂ or the reaction of lipids with reactive oxygen species (ROS) such as HOCl. Another explanation of increased LPC concentration is the decreased re-acylation of LPC into PC. While there are also several other lysophospholipids, LPC is the most abundant lysophospholipid in mammals and will therefore be the focus of this review. LPC is involved in many physiological processes. It induces the migration of lymphocytes, fostering the production of pro-inflammatory compounds by inducing oxidative stress. LPC also "signals" via G protein-coupled and Toll-like receptors and has been implicated in the development of different diseases. However, LPCs are not purely "bad": this is reflected by the fact that the concentration and fatty acyl composition of LPC varies under different conditions, in plasma of healthy and diseased individuals, in tissues and different tumors. Targeting LPC and lipid metabolism and restoring homeostasis might be a potential therapeutic method for inflammation-related diseases.

磷脂（PL）是细胞膜的主要成分，磷脂代谢的变化与多种疾病的发病机制有关。尤其是溶血磷脂酰胆碱（LPC），它是氧化损伤组织中含量相当丰富的一种成分。溶血磷脂酰胆碱来源于磷脂酶 A2 对磷脂酰胆碱（PC）的裂解或脂质与活性氧（ROS）（如 HOCl）的反应。LPC 浓度升高的另一个原因是 LPC 转化为 PC 的再酰化减少。虽然还有其他几种溶血磷脂，但 LPC 是哺乳动物体内含量最高的溶血磷脂，因此将是本综述的重点。LPC 参与了许多生理过程。它能诱导淋巴细胞迁移，通过诱导氧化应激促进促炎化合物的产生。LPC 还通过 G 蛋白偶联受体和 Toll 样受体发出 "信号"，并与不同疾病的发生发展有关。然而，LPC 并不纯粹是 "坏 "的：LPC 的浓度和脂肪酰基组成在不同条件下、在健康人和病人的血浆中、在组织和不同肿瘤中都会发生变化，就反映了这一点。针对 LPC 和脂质代谢以及恢复平衡可能是治疗炎症相关疾病的一种潜在方法。

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引用次数: 0

Treatment with APAC, a dual antiplatelet anticoagulant heparin proteoglycan mimetic, limits early collar-induced carotid atherosclerotic plaque development in Apoe−/− mice APAC是一种双重抗血小板抗凝剂肝素蛋白多糖模拟物，它能限制载脂蛋白/-小鼠颈动脉粥样硬化斑块的早期发展。

IF 4.9 2区医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS

Atherosclerosis

Pub Date : 2024-08-22 DOI: 10.1016/j.atherosclerosis.2024.118567

Background and aims

Mast cell-derived heparin proteoglycans (HEP-PG) can be mimicked by bioconjugates carrying antithrombotic and anti-inflammatory properties. The dual antiplatelet and anticoagulant (APAC) construct administered, either locally or intravenously (i.v.), targets activated endothelium, its adhesion molecules, and subendothelial matrix proteins, all relevant to atherogenesis. We hypothesized that APAC influences cellular interactions in atherosclerotic lesion development and studied APAC treatment during the initiation and progression of experimental atherosclerosis.

Methods

Male western-type diet-fed Apoe^−/− mice were equipped with perivascular carotid artery collars to induce local atherosclerosis. In this model, mRNA expression of adhesion molecules including ICAM-1, VCAM-1, P-Selectin, and Platelet Factor 4 (PF4) are upregulated upon lesion development. From day 1 (prevention) or from 2.5 weeks after lesion initiation (treatment), mice were administered 0.2 mg/kg APAC i.v. or control vehicle three times weekly for 2.5 weeks. At week 5 after collar placement, mice were sacrificed, and lesion morphology was microscopically assessed.

Results

APAC treatment did not affect body weight or plasma total cholesterol levels during the experiments. In the prevention setting, APAC reduced carotid artery plaque size and volume by over 50 %, aligning with decreased plaque macrophage area and collagen content. During the treatment setting, APAC reduced macrophage accumulation and necrotic core content, and improved markers of plaque stability.

Conclusions

APAC effectively reduced early atherosclerotic lesion development and improved markers of plaque inflammation in advanced atherosclerosis. Thus, APAC may have potential to alleviate the progression of atherosclerosis.

背景和目的：肥大细胞衍生的肝素蛋白多糖（HEP-PG）可被具有抗血栓和抗炎特性的生物共轭物模拟。局部或静脉注射的双重抗血小板和抗凝剂（APAC）构建物针对的是活化的内皮、其粘附分子和内皮下基质蛋白，这些都与动脉粥样硬化有关。我们假设 APAC 会影响动脉粥样硬化病变发展过程中的细胞相互作用，并在实验性动脉粥样硬化的起始和发展过程中对 APAC 治疗进行了研究：方法：雄性西式饮食喂养的载脂蛋白/-小鼠装有血管周围颈动脉袢以诱导局部动脉粥样硬化。在该模型中，病变发生时粘附分子（包括 ICAM-1、VCAM-1、P-选择素和血小板因子 4 (PF4)）的 mRNA 表达上调。从病变开始的第 1 天（预防）或 2.5 周后（治疗）起，给小鼠静脉注射 0.2 mg/kg APAC 或对照药物，每周三次，持续 2.5 周。放置颈圈后第5周，小鼠被处死，并在显微镜下评估病变形态：结果：在实验过程中，APAC治疗不会影响体重或血浆总胆固醇水平。在预防阶段，APAC可使颈动脉斑块的大小和体积缩小50%以上，同时斑块巨噬细胞面积和胶原蛋白含量也有所减少。在治疗过程中，APAC减少了巨噬细胞的聚集和坏死核心的含量，并改善了斑块稳定性的指标：结论：APAC能有效减少早期动脉粥样硬化病变的发展，并改善晚期动脉粥样硬化斑块的炎症指标。因此，APAC 有可能缓解动脉粥样硬化的进展。

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引用次数: 0

Sex differences in plaque characteristics of fractional flow reserve-negative non-culprit lesions after myocardial infarction 心肌梗死后分数血流储备阴性非病灶斑块特征的性别差异。

IF 4.9 2区医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS

Atherosclerosis

Pub Date : 2024-08-22 DOI: 10.1016/j.atherosclerosis.2024.118568

Background and aims

Recurrent events after myocardial infarction (MI) are common and often originate from native non-culprit (NC) lesions that are non-flow limiting. These lesions consequently pose as targets to improve long-term outcome. It is, however, largely unknown whether these lesions differ between sexes. The aim of this study was to assess such potential differences.

Methods

From the PECTUS-obs study, we assessed sex-related differences in plaque characteristics of fractional flow reserve (FFR)-negative intermediate NC lesions in 420 MI-patients.

Results

Among the included patients, 80 (19.1 %) were female and 340 (80.9 %) male. Women were older and more frequently had hypertension and diabetes. In total, 494 NC lesions were analyzed. After adjustment for clinical characteristics and accounting for within-patients clustering, lesion length was longer in female patients (20.8 ± 10.0 vs 18.3 ± 8.5 mm, p = 0.048) and minimum lumen area (2.30 ± 1.42 vs 2.78 ± 1.54 mm², p < 0.001) and minimum lumen diameter (1.39 ± 0.45 vs 1.54 ± 0.44 mm, p < 0.001) were smaller. The minimum fibrous cap thickness was smaller among females (96 ± 53 vs 112 ± 72 μm, p = 0.025), with more lesions harboring a thin cap fibroatheroma (39.3 % vs 24.9 %, p < 0.001). Major adverse cardiovascular events at two years occurred in 6.3 % of female patients and 11.8 % of male patients (p = 0.15).

Conclusions

FFR-negative NC lesions after MI harbored more high-risk plaque features in female patients. Although this did not translate into an excess of recurrent events in female patients in this modestly sized cohort, it remains to be investigated whether this difference affects clinical outcome.

背景和目的：心肌梗死（MI）后复发的情况很常见，而且往往源于非血流受限的原发性非梗死（NC）病变。因此，这些病变是改善长期预后的目标。然而，这些病变在性别上是否存在差异在很大程度上还是个未知数。本研究旨在评估这种潜在的差异：方法：在 PECTUS-obs 研究中，我们评估了 420 名心肌梗死患者中分数血流储备（FFR）阴性的中间 NC 病变斑块特征中与性别相关的差异：在纳入的患者中，80 名（19.1%）为女性，340 名（80.9%）为男性。女性年龄更大，患有高血压和糖尿病的更多。共分析了 494 例 NC 病变。在对临床特征进行调整并考虑患者内部聚类因素后，女性患者的病变长度（20.8 ± 10.0 vs 18.3 ± 8.5 mm，p = 0.048）和最小管腔面积（2.30 ± 1.42 vs 2.78 ± 1.54 mm2，p 结论：女性患者的病变长度和最小管腔面积均大于男性：女性患者心肌梗死后 FFR 阴性的 NC 病变具有更多的高风险斑块特征。虽然在这个规模不大的队列中，女性患者的复发率并没有因此而增加，但这种差异是否会影响临床结果仍有待研究。

{"title":"Sex differences in plaque characteristics of fractional flow reserve-negative non-culprit lesions after myocardial infarction","authors":"","doi":"10.1016/j.atherosclerosis.2024.118568","DOIUrl":"10.1016/j.atherosclerosis.2024.118568","url":null,"abstract":"<div><h3>Background and aims</h3><p>Recurrent events after myocardial infarction (MI) are common and often originate from native non-culprit (NC) lesions that are non-flow limiting. These lesions consequently pose as targets to improve long-term outcome. It is, however, largely unknown whether these lesions differ between sexes. The aim of this study was to assess such potential differences.</p></div><div><h3>Methods</h3><p>From the PECTUS-obs study, we assessed sex-related differences in plaque characteristics of fractional flow reserve (FFR)-negative intermediate NC lesions in 420 MI-patients.</p></div><div><h3>Results</h3><p>Among the included patients, 80 (19.1 %) were female and 340 (80.9 %) male. Women were older and more frequently had hypertension and diabetes. In total, 494 NC lesions were analyzed. After adjustment for clinical characteristics and accounting for within-patients clustering, lesion length was longer in female patients (20.8 ± 10.0 <em>vs</em> 18.3 ± 8.5 mm, <em>p</em> = 0.048) and minimum lumen area (2.30 ± 1.42 <em>vs</em> 2.78 ± 1.54 mm<sup>2</sup>, <em>p</em> < 0.001) and minimum lumen diameter (1.39 ± 0.45 <em>vs</em> 1.54 ± 0.44 mm, <em>p</em> < 0.001) were smaller. The minimum fibrous cap thickness was smaller among females (96 ± 53 <em>vs</em> 112 ± 72 μm, <em>p</em> = 0.025), with more lesions harboring a thin cap fibroatheroma (39.3 % <em>vs</em> 24.9 %, <em>p</em> < 0.001). Major adverse cardiovascular events at two years occurred in 6.3 % of female patients and 11.8 % of male patients (<em>p</em> = 0.15).</p></div><div><h3>Conclusions</h3><p>FFR-negative NC lesions after MI harbored more high-risk plaque features in female patients. Although this did not translate into an excess of recurrent events in female patients in this modestly sized cohort, it remains to be investigated whether this difference affects clinical outcome.</p></div>","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":null,"pages":null},"PeriodicalIF":4.9,"publicationDate":"2024-08-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0021915024011407/pdfft?md5=8fbe71f2004a86cb3f38808c6f6e1cbb&pid=1-s2.0-S0021915024011407-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142145003","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}

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