Atherosclerosis最新文献

英文中文

Lipids associated with atherosclerotic plaque instability revealed by mass spectrometry imaging of human carotid arteries 人体颈动脉质谱成像揭示与动脉粥样硬化斑块不稳定性有关的脂质

IF 4.9 2区医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS

Atherosclerosis

Pub Date : 2024-08-07 DOI: 10.1016/j.atherosclerosis.2024.118555

Francesco Greco , Giulia Bertagna , Laura Quercioli , Angela Pucci , Silvia Rocchiccioli , Mauro Ferrari , Fabio A. Recchia , Liam A. McDonnell

Background and aims

Lipids constitute one of the main components of atherosclerosis lesions and are the mediators of many mechanisms involved in plaque progression and stability. Here we tested the hypothesis that lipids known to be involved in plaque development exhibited associations with plaque vulnerability. We used spatial lipidomics to overcome plaque heterogeneity and to compare lipids from specific regions of symptomatic and asymptomatic human carotid atherosclerotic plaques.

Methods

Carotid atherosclerotic plaques were collected from symptomatic and asymptomatic patients. Plaque lipids were analyzed with the spatial lipidomics technique matrix-assisted laser desorption/ionization mass spectrometry imaging, and histology and immunofluorescence were used to segment the plaques into histomolecularly distinct regions.

Results

Macrophage-rich regions from symptomatic lesions were found to be enriched in phosphatidylcholines (synthesized to counteract excess free cholesterol), while the same region from asymptomatic plaques were enriched in polyunsaturated cholesteryl esters and triglycerides, characteristic of functional lipid droplets. Vascular smooth muscle cells (VSMCs) of the fibrous cap of asymptomatic plaques were enriched in lysophosphatidylcholines and cholesteryl esters, know to promote VSMC proliferation and migration, crucial for the buildup of the fibrous cap stabilizing the plaque.

Conclusions

The investigation of the region-specific lipid composition of symptomatic and asymptomatic human atherosclerotic plaques revealed specific lipid markers of plaque outcome, which could be linked to known biological characteristics of stable plaques.

背景和目的脂质是动脉粥样硬化病变的主要成分之一，是斑块进展和稳定过程中许多机制的介质。在这里，我们检验了一个假设，即已知参与斑块发展的脂质与斑块的易损性有关。我们使用空间脂质组学来克服斑块的异质性，并比较有症状和无症状人类颈动脉粥样硬化斑块特定区域的脂质。用空间脂质组学技术基质辅助激光解吸电离质谱成像分析斑块脂质，并用组织学和免疫荧光将斑块分割成不同的组织分子区域。结果发现无症状病变中富含巨噬细胞的区域富含磷脂酰胆碱（合成磷脂酰胆碱是为了抵消过量的游离胆固醇），而无症状斑块中富含多不饱和胆固醇酯和甘油三酯，这是功能性脂滴的特征。无症状斑块纤维帽的血管平滑肌细胞（VSMC）富含溶血磷脂酰胆碱和胆固醇酯，这些物质可促进血管平滑肌细胞的增殖和迁移，对纤维帽的形成和斑块的稳定至关重要。

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引用次数: 0

HDL cholesterol efflux capacity and cholesterol loading capacity in long-term fasting: Evidence from a prospective, single-arm interventional study in healthy individuals 长期禁食的高密度脂蛋白胆固醇外流能力和胆固醇负荷能力：一项针对健康人的前瞻性单臂干预研究提供的证据

IF 4.9 2区医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS

Atherosclerosis

Pub Date : 2024-08-06 DOI: 10.1016/j.atherosclerosis.2024.118548

Franziska Grundler , Marcella Palumbo , Maria Pia Adorni , Francesca Zimetti , Bianca Papotti , Dietmar Plonné , Alfred Holley , Robin Mesnage , Massimiliano Ruscica , Françoise Wilhelmi de Toledo

Background and aims

Long-term fasting (LF) is increasingly emerging as a non-pharmacological approach to modulate risk factors associated with the development of atherosclerotic cardiovascular diseases (ASCVD). However, protection from ASCVD is more tied to the functionality of high-density lipoprotein (HDL) than its plasma levels. Our prospective interventional study focuses on the functional properties of lipoproteins in modulating cholesterol homeostasis on peripheral cells and examines how LF may influence this and lipoprotein subclass composition. For that purpose, we investigated its impact on HDL-cholesterol efflux capacity (CEC), and on serum cholesterol loading capacity (CLC).

Methods

Forty healthy subjects (50 % females) underwent medically supervised 9-day fasting (250 kcal/day) in a specialised facility. Thirty-two subjects had a follow-up examination after one month of food reintroduction.

Results

LF was well tolerated and increased self-reported energy levels. Fasting reduced triglycerides (TG), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C) and HDL cholesterol (HDL-C). Very-low-density lipoprotein cholesterol (VLDL-C) and LDL3-C showed sustained reductions at follow-up. Only HDL-C, specifically HDL2-C levels, increased at follow-up. Total HDL-CEC decreased during LF and increased above baseline at follow-up. Fasting decreased ATP binding cassette (ABC)A1-mediated HDL-CEC whereas ABCG1-mediated HDL-CEC remained unaffected. Aqueous diffusion increased at follow up. LF decreased serum CLC and then returned to baseline levels.

Conclusions

LF not only maintains lipoprotein functionality but also contributes to a favorable shift in the atherogenic risk profile, which persists even after food reintroduction. This further emphasizes the importance of considering HDL functionality alongside traditional lipid measurements to understand the potential for non-pharmacological interventions like LF to promote cardiovascular prevention and health.

Trial registration number

NCT05031598.

背景和目的长期禁食（LF）正逐渐成为一种非药物方法，用于调节与动脉粥样硬化性心血管疾病（ASCVD）发展相关的风险因素。然而，防止动脉粥样硬化性心血管疾病更多地与高密度脂蛋白（HDL）的功能而不是其血浆水平有关。我们的前瞻性干预研究侧重于脂蛋白在调节外周细胞胆固醇稳态方面的功能特性，并探讨低密度脂蛋白如何影响脂蛋白亚类的组成。为此，我们研究了低密度脂蛋白对高密度脂蛋白胆固醇外排能力（CEC）和血清胆固醇负荷能力（CLC）的影响。32名受试者在重新摄入食物一个月后接受了随访检查。空腹降低了甘油三酯（TG）、总胆固醇（TC）、低密度脂蛋白胆固醇（LDL-C）和高密度脂蛋白胆固醇（HDL-C）。极低密度脂蛋白胆固醇（VLDL-C）和低密度脂蛋白胆固醇（LDL3-C）在随访中持续下降。只有高密度脂蛋白胆固醇（尤其是高密度脂蛋白2-C水平）在随访中有所增加。总 HDL-CEC 在 LF 期间下降，在随访时高于基线。空腹会降低 ATP 结合盒 (ABC)A1 介导的 HDL-CEC，而 ABCG1 介导的 HDL-CEC 则不受影响。随访时，水扩散增加。结论低脂蛋白不仅能维持脂蛋白的功能，还能促使致动脉粥样硬化风险发生有利的转变，这种转变甚至在重新引入食物后仍然存在。这进一步强调了在进行传统血脂测量的同时考虑高密度脂蛋白功能的重要性，以了解低密度脂蛋白等非药物干预措施在促进心血管预防和健康方面的潜力。

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引用次数: 0

CRISPR/Cas9-mediated suppression of A4GALT rescues endothelial cell dysfunction in a fabry disease vasculopathy model derived from human induced pluripotent stem cells CRISPR/Cas9 介导的 A4GALT 抑制可挽救由人类诱导多能干细胞衍生的法布里病血管病变模型中的内皮细胞功能障碍

IF 4.9 2区医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS

Atherosclerosis

Pub Date : 2024-08-02 DOI: 10.1016/j.atherosclerosis.2024.118549

Yoo Jin Shin , Seung Yun Chae , Hanbi Lee , Xianying Fang , Sheng Cui , Sun Woo Lim , Kang In Lee , Jae Young Lee , Can Li , Chul Woo Yang , Byung Ha Chung

Background and aims

The objective of this study was to investigate the efficacy of CRISPR/Cas9-mediated A4GALT suppression in rescuing endothelial dysfunction in Fabry disease (FD) endothelial cells (FD-ECs) derived from human induced pluripotent stem cells (hiPSCs).

Methods

We differentiated hiPSCs (WT (wild-type), WTC-11), GLA-mutant hiPSCs (GLA-KO, CMC-Fb-002), and CRISPR/Cas9-mediated A4GALT-KO hiPSCs (GLA/A4GALT-KO, Fb-002-A4GALT-KO) into ECs and compared FD phenotypes and endothelial dysfunction. We also analyzed the effect of A4GALT suppression on reactive oxygen species (ROS) formation and transcriptome profiles through RNA sequencing.

Results

GLA-mutant hiPSC-ECs (GLA-KO and CMC-Fb-002) showed downregulated expression of EC markers and significantly reduced α-GalA expression with increased Gb-3 deposition and intra-lysosomal inclusion bodies. However, CRISPR/Cas9-mediated A4GALT suppression in GLA/A4GALT-KO and Fb-002-A4GALT-KO hiPSC-ECs increased expression levels of EC markers and rescued these FD phenotypes. GLA-mutant hiPSC-ECs failed to form tube-like structure in tube formation assays, showing significantly decreased migration of cells into the scratched wound area. In contrast, A4GALT suppression improved tube formation and cell migration capacity. Western blot analysis revealed that MAPK and AKT phosphorylation levels were downregulated while SOD and catalase were upregulated in GLA-KO hiPSC-ECs. However, suppression of A4GALT restored these protein alterations. RNA sequencing analysis demonstrated significant transcriptome changes in GLA-mutant EC, especially in angiogenesis, cell death, and cellular response to oxidative stress. However, these were effectively restored in GLA/A4GALT-KO hiPSC-ECs.

Conclusions

CRISPR/Cas9-mediated A4GALT suppression rescued FD phenotype and endothelial dysfunction in GLA-mutant hiPSC-ECs, presenting a potential therapeutic approach for FD-vasculopathy.

背景和目的本研究的目的是调查 CRISPR/Cas9 介导的 A4GALT 抑制在挽救法布里病（FD）内皮细胞（FD-ECs）的内皮功能障碍方面的疗效，这些细胞来源于人类诱导多能干细胞（hiPSCs）。方法我们将hiPSCs（WT（野生型），WTC-11）、GLA突变型hiPSCs（GLA-KO，CMC-Fb-002）和CRISPR/Cas9介导的A4GALT-KO hiPSCs（GLA/A4GALT-KO，Fb-002-A4GALT-KO）分化成ECs，并比较了FD表型和内皮功能障碍。结果GLA突变的hiPSC-ECs（GLA-KO和CMC-Fb-002）显示EC标志物表达下调，α-GalA表达显著减少，Gb-3沉积和溶酶体内包涵体增加。然而，在GLA/A4GALT-KO和Fb-002-A4GALT-KO hiPSC-EC中，CRISPR/Cas9介导的A4GALT抑制提高了EC标记物的表达水平，并挽救了这些FD表型。GLA突变的hiPSC-EC在管形成试验中未能形成管状结构，显示细胞向划伤伤口区域的迁移显著减少。相比之下，抑制A4GALT可改善管状结构的形成和细胞迁移能力。Western印迹分析显示，在GLA-KO hiPSC-ECs中，MAPK和AKT磷酸化水平下调，而SOD和过氧化氢酶上调。然而，抑制A4GALT可恢复这些蛋白质变化。RNA测序分析表明，GLA突变型EC的转录组发生了显著变化，尤其是在血管生成、细胞死亡和细胞对氧化应激的反应方面。结论CRISPR/Cas9介导的A4GALT抑制挽救了GLA突变型hiPSC-EC的FD表型和内皮功能障碍，为FD-血管病变提供了一种潜在的治疗方法。

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引用次数: 0

Therapeutic efficacy of peptide vaccine (AtheroVax) in an animal model of chronic inflammation 多肽疫苗（AtheroVax）在慢性炎症动物模型中的治疗效果

IF 4.9 2区医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS

Atherosclerosis

Pub Date : 2024-08-01 DOI: 10.1016/j.atherosclerosis.2024.118288

Nickolas Kipshidze , George Dangas , Jawed Fareed , Zurab Kakabadze , Teona Paresishvili , Nn Kipshidze , Patrick Iversen

引用次数: 0

DOT1L-AF10 mediated H3K79me3 regulates inflammatory switch of endothelial cells in D-Flow DOT1L-AF10 介导的 H3K79me3 调节 D-流动中内皮细胞的炎症转换

IF 4.9 2区医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS

Atherosclerosis

Pub Date : 2024-08-01 DOI: 10.1016/j.atherosclerosis.2024.118251

Yash Katakia, Ritobrata Bhattacharyya, Nehal Gupta, Nivedha Suresh, Syamantak Majumder

引用次数: 0

Sex-specific plasma-proteome of incident coronary artery disease 冠心病发病的性别特异性血浆蛋白组

IF 4.9 2区医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS

Atherosclerosis

Pub Date : 2024-08-01 DOI: 10.1016/j.atherosclerosis.2024.118507

Vincent Sier, Diana Van Heemst, Ko Willems Van Dijk, Raymond Noordam, Margreet De Vries

引用次数: 0

Impact of loss-of-function in angiopoietin-like 4 on the human phenome 血管生成素样 4 功能缺失对人类表型的影响

IF 4.9 2区医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS

Atherosclerosis

Pub Date : 2024-08-01 DOI: 10.1016/j.atherosclerosis.2024.118497

Eloi Gagnon, Jérôme Bourgault, Benoit Arsenault

引用次数: 0

Lipid-induced ATF4 signalling impairs macrophage efferocytosis and promotes atherosclerotic plaque necrosis 脂质诱导的 ATF4 信号损害巨噬细胞的排泄功能并促进动脉粥样硬化斑块坏死

IF 4.9 2区医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS

Atherosclerosis

Pub Date : 2024-08-01 DOI: 10.1016/j.atherosclerosis.2024.118481

Aarushi Singhal , Umesh Dhawan , Kunzangla Bhutia , Heather Wilson , Guillermo Velasco , Endre Kiss-Toth , Manikandan Subramanian

引用次数: 0

Lesion site-specific proteomics reveals that necrotic core and fibrous cap have the strongest association with human carotid plaque stability 病变部位特异性蛋白质组学发现，坏死核心和纤维帽与人体颈动脉斑块的稳定性关系最为密切

IF 4.9 2区医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS

Atherosclerosis

Pub Date : 2024-08-01 DOI: 10.1016/j.atherosclerosis.2024.118487

Ankit Sinha , Nadja Sachs , Elena Kratz , Jessica Pauli , Sophia Steigerwald , Vincent Albrecht , Thierry Nordmann , Hanna Winter , Lars Maegdefessel , Matthias Mann

引用次数: 0

A genome-wide screen to decipher regulation of membrane saturation in mammalian cells using a novel fluorescent reporter 利用新型荧光报告器进行全基因组筛选，破解哺乳动物细胞膜饱和度的调控机制

IF 4.9 2区医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS

Atherosclerosis

Pub Date : 2024-08-01 DOI: 10.1016/j.atherosclerosis.2024.118269

Andrej Gorbatenko , Noam Zelcer

引用次数: 0

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Atherosclerosis

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