Atherosclerosis最新文献_第5页

Unmasking the genetic double agents of hyperglycemia: Mendelian randomization in endotheli-hell espionage 揭示高血糖的遗传双重因素：内皮-地狱间谍的孟德尔随机化。

IF 5.7 2区医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS

Atherosclerosis

Pub Date : 2025-11-01 DOI: 10.1016/j.atherosclerosis.2025.120506

Shivangi Pande , Fahimeh Varzideh , George Ishak , Pasquale Mone , Urna Kansakar , Stanislovas S. Jankauskas , Gaetano Santulli

引用次数: 0

Targeting LDL aggregation decreases atherosclerotic lipid burden in a humanized mouse model of familial hypercholesterolemia: Crucial role of ApoB100 conformational stabilization 在家族性高胆固醇血症人源化小鼠模型中，以低密度脂蛋白聚集为靶点可降低动脉粥样硬化的脂质负担：ApoB100 构象稳定的关键作用。

IF 5.7 2区医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS

Atherosclerosis

Pub Date : 2025-11-01 DOI: 10.1016/j.atherosclerosis.2024.118630

A. Benitez-Amaro , E. Garcia , M.T. La Chica Lhoëst , A. Martínez , C. Borràs , M. Tondo , M.V. Céspedes , P. Caruana , A. Pepe , B. Bochicchio , A. Cenarro , F. Civeira , R. Prades , J.C. Escola-Gil , V. Llorente-Cortés

Background and aims

Low-density lipoprotein (LDL) aggregation is nowadays considered a therapeutic target in atherosclerosis. DP3, the retro-enantio version of the sequence Gly¹¹²⁷-Cys¹¹⁴⁰ of LRP1, efficiently inhibits LDL aggregation and foam cell in vitro formation. Here, we investigate whether DP3 modulates atherosclerosis in a humanized ApoB100, LDL receptor (LDLR) knockout mice (Ldlr^−/−hApoB100 Tg) and determine the potential LDL-related underlying mechanisms.

Methods

Tg mice were fed an HFD for 21 days to induce atherosclerosis and then randomized into three groups that received a daily subcutaneous administration (10 mg/kg) of i) vehicle, ii) DP3 peptide, or iii) a non-active peptide (IP321). The in vivo biodistribution of a fluorescent-labeled peptide version (TAMRA-DP3), and its colocalization with ApoB100 in the arterial intima, was analyzed by imaging system (IVIS) and confocal microscopy. Heart aortic roots were used for atherosclerosis detection and quantification. LDL functionality was analyzed by biochemical, biophysical, molecular, and cellular studies.

Results

Intimal neutral lipid accumulation in the aortic root was reduced in the DP3-treated group as compared to control groups. ApoB100 in LDLs from the DP3 group exhibited an increased percentage of α-helix secondary structures and decreased immunoreactivity to anti-ApoB100 antibodies. LDL from DP3-treated mice were protected against passive and sphingomyelinase (SMase)-induced aggregation, although they still experienced SMase-induced sphingomyelin phospholysis. In patients with familial hypercholesterolemia (FH), DP3 efficiently inhibited both SMase-induced phospholysis and aggregation.

Conclusions

DP3 peptide administration inhibits atherosclerosis by preserving the α-helix secondary structures of ApoB100 in a humanized ApoB100 murine model that mimicks the hallmark of human hypercholesterolemia.

背景和目的：低密度脂蛋白（LDL）聚集如今被认为是动脉粥样硬化的治疗靶点。DP3是LRP1的Gly1127-Cys1140序列的逆对映版本，能有效抑制低密度脂蛋白的聚集和体外泡沫细胞的形成。在此，我们研究了DP3是否能调节人源化载脂蛋白B100、低密度脂蛋白受体（LDLR）基因敲除小鼠（Ldlr-/-hApoB100 Tg）的动脉粥样硬化，并确定了潜在的低密度脂蛋白相关潜在机制：给Tg小鼠喂食高密度脂蛋白膳食（HFD）21天以诱发动脉粥样硬化，然后随机分为三组，每组每天皮下注射（10毫克/千克）i）载体、ii）DP3肽或iii）非活性肽（IP321）。通过成像系统（IVIS）和共聚焦显微镜分析了荧光标记肽版本（TAMRA-DP3）的体内生物分布及其与动脉内膜中载脂蛋白B100的共定位。心脏主动脉根部用于动脉粥样硬化的检测和量化。通过生化、生物物理、分子和细胞研究分析了低密度脂蛋白的功能：结果：与对照组相比，DP3 治疗组主动脉根部内膜中性脂质堆积减少。DP3组低密度脂蛋白中载脂蛋白B100的α-螺旋二级结构比例增加，抗载脂蛋白B100抗体的免疫活性降低。经DP3处理的小鼠的低密度脂蛋白对被动和鞘磷脂酶（SMase）诱导的聚集具有保护作用，尽管它们仍经历了SMase诱导的鞘磷脂磷酸化。在家族性高胆固醇血症（FH）患者中，DP3能有效抑制SM酶诱导的磷酸化和聚集：结论：在模拟人类高胆固醇血症特征的人源化载脂蛋白100小鼠模型中，DP3肽通过保留载脂蛋白100的α-螺旋二级结构抑制动脉粥样硬化。

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引用次数: 0

Sex differences in cholesterol levels among prepubertal children 青春期前儿童胆固醇水平的性别差异。

IF 5.7 2区医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS

Atherosclerosis

Pub Date : 2025-11-01 DOI: 10.1016/j.atherosclerosis.2025.120484

Jan Kafol , Mia Becker , Barbara Cugalj Kern , Jaka Sikonja , Matej Mlinaric , Katarina Sedej , Matej Kafol , Ana Drole Torkar , Jernej Kovac , Tadej Battelino , Urh Groselj

Background and aims

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).

Methods

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.

Results

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).

Conclusion

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.

背景和目的：胆固醇水平的性别差异在成人和青少年中有很好的记录，但在青春期前儿童中存在的数据有限。本研究旨在评估青春期前儿童总胆固醇（TC）和低密度脂蛋白胆固醇（LDL-C）水平的先天性别差异，包括普通人群和家族性高胆固醇血症（FH）患者。方法：这项横断面研究使用了斯洛文尼亚全民FH筛查项目的数据。2014年（N = 3412）和2023年（N = 4182）选取了两组随机抽样的5岁儿童进行常规胆固醇筛查。此外，来自斯洛文尼亚高胆固醇血症登记处的参考队列（n = 1160，年龄）结果：在2014年和2023年的队列中，女孩的TC水平明显高于男孩（中位数差异：0.10-0.11 mmol/L; p）结论：青春期前女孩的TC和LDL-C水平略高于男孩，在青春期前FH阳性儿童中未观察到这种差异，这表明致病性FH变异的存在可能超越了脂质代谢的先天生理差异。这些发现支持普遍的早期胆固醇筛查，并提示性别特异性参考值可能改善青春期前fh阴性儿童的早期心血管风险评估。

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引用次数: 0

Global, regional and national burden of ischemic heart disease attributable to ambient fine particulate matter pollution from 1990 to 2021, with predictions to 2072: An analysis of the global burden of disease study 2021 1990年至2021年环境细颗粒物污染导致的全球、区域和国家缺血性心脏病负担，并预测到2072年：2021年全球疾病负担研究分析

IF 5.7 2区医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS

Atherosclerosis

Pub Date : 2025-11-01 DOI: 10.1016/j.atherosclerosis.2025.120498

Enyu Tong , Yiming Chen , Chuanzhong Chen , Fengying Zhang , Thomas Krafft

Background and aims

To assess the global burden of ischemic heart disease (IHD) attributable to ambient PM_2.5 pollution, including trends, geographic disparities, demographic drivers, and future projections.

Methods

Using Global Burden of Diseases (GBD) 2021 data, we quantified PM_2.5-related IHD deaths and disability-adjusted life years (DALYs). Decomposition analysis identified demographic drivers (population growth, aging, and epidemiological changes), and projection models estimated 50-year trends in age-standardized mortality and DALY rates.

Results

In 2021, ambient PM_2.5 caused 2.4 million deaths and 54.7 million DALYs globally. Although PM_2.5-attributable IHD burden declined from 1990 to 2021, mortality and DALY rates stayed disproportionately high because population growth and aging increased the overall burden. The burden of ischemic heart disease attributable to ambient PM_2.5 is projected to continue rising over the next 50 years.

Conclusions

This study highlights the association between ambient PM_2.5 pollution and IHD, particularly in low- and middle-income regions, males, and older populations, and indicates that age-standardized mortality and DALY rates are projected to rise. Monitoring exposure and implementing targeted strategies for these susceptible groups to address these inequities are critically important.

背景和目的：评估由环境PM2.5污染引起的缺血性心脏病（IHD）的全球负担，包括趋势、地理差异、人口驱动因素和未来预测。方法：使用全球疾病负担（GBD） 2021数据，我们量化了pm2.5相关的IHD死亡和残疾调整生命年（DALYs）。分解分析确定了人口驱动因素（人口增长、老龄化和流行病学变化），预测模型估计了年龄标准化死亡率和DALY率的50年趋势。结果：2021年，全球环境PM2.5造成240万人死亡，5470万人伤残调整年。虽然1990年至2021年期间pm2.5导致的IHD负担有所下降，但由于人口增长和老龄化增加了总体负担，死亡率和DALY率仍然高得不成比例。预计在未来50年，由环境PM2.5引起的缺血性心脏病负担将继续上升。结论：本研究强调了环境PM2.5污染与IHD之间的关联，特别是在低收入和中等收入地区、男性和老年人群中，并表明年龄标准化死亡率和DALY率预计将上升。监测这些易受影响群体的暴露情况并实施有针对性的战略，以解决这些不平等现象，这一点至关重要。

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引用次数: 0

Ethnic differences in HDL quantity, quality, and potential associations with coronary heart disease risk HDL数量、质量的种族差异及其与冠心病风险的潜在关联

IF 5.7 2区医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS

Atherosclerosis

Pub Date : 2025-11-01 DOI: 10.1016/j.atherosclerosis.2025.120565

Sabrina Scilletta , Paul Welsh , Jack David Beazer , Antonino Di Pino , Naveed Sattar

Background and aims

Ethnic differences in HDL cholesterol (HDL-c) may help explain disparities in coronary heart disease (CHD) risk, but the clinical interpretation of HDL-c and its metabolomic subfractions across populations remains unclear.

Methods

We examined HDL quantity and quality in relation to ethnicity and CHD risk in UK Biobank. HDL-c and ten metabolomic HDL measures (reflecting particle size and lipid composition) were analyzed in relation to CHD using Cox models stratified by ethnicity. Linear regression assessed differences in HDL-c by ethnicity. Models were sequentially adjusted for sociodemographic, clinical, adiposity, and physical activity variables.

Results

After adjustment, HDL-c concentrations were modestly lower in South Asian (−0.091 mmol/L) and Black (−0.025 mmol/L) participants compared to White participants. These differences were substantially attenuated after further adjustment for adiposity and physical activity. HDL-c was inversely associated with CHD across all ethnic groups, with the strongest association in South Asian (HR per SD: 0.40 [0.29–0.54]) compared with White participants (HR: 0.64 [0.61–0.67]). Several HDL subfractions (particularly large HDL particles and average HDL diameter) showed stronger inverse associations with CHD in South Asian participants compared to other ethnic groups.

Conclusions

Lower HDL-c concentrations in South Asian and Black vs White participants appear largely driven by differential physical activity and/or adiposity measures. In South Asian individuals, HDL quantity and quality measures may be more strongly predictive of risk, warranting further investigation into their clinical and biological utility in diverse populations.

背景和目的高密度脂蛋白胆固醇（HDL-c）的种族差异可能有助于解释冠心病（CHD）风险的差异，但高密度脂蛋白胆固醇及其代谢组亚组分在人群中的临床解释尚不清楚。方法：我们在英国生物库中检测HDL的数量和质量与种族和冠心病风险的关系。使用按种族分层的Cox模型分析HDL-c和10种代谢组学HDL测量值（反映颗粒大小和脂质组成）与冠心病的关系。线性回归评估不同种族的HDL-c差异。根据社会人口学、临床、肥胖和身体活动变量依次调整模型。调整后，与白人受试者相比，南亚受试者（- 0.091 mmol/L）和黑人受试者（- 0.025 mmol/L）的HDL-c浓度略低。在进一步调整肥胖和体力活动因素后，这些差异显著减弱。HDL-c与冠心病呈负相关，与白人受试者（HR: 0.64[0.61-0.67]）相比，南亚受试者（HR / SD: 0.40[0.29-0.54]）的相关性最强。与其他种族相比，南亚参与者的一些HDL亚组分（特别是大HDL颗粒和平均HDL直径）与冠心病表现出更强的负相关。南亚和黑人与白人参与者中较低的HDL-c浓度似乎主要是由不同的体力活动和/或肥胖措施引起的。在南亚个体中，高密度脂蛋白的数量和质量测量可能更能预测风险，因此有必要进一步研究其在不同人群中的临床和生物学效用。

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引用次数: 0

Smogged arteries, sneaky killers 浑浊的动脉，狡猾的杀手。

IF 5.7 2区医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS

Atherosclerosis

Pub Date : 2025-11-01 DOI: 10.1016/j.atherosclerosis.2025.120519

Jacques D. Barth (Editorial)

This editorial highlights a groundbreaking study by Enyo Tong and colleagues, published in Atherosclerosis, which examines the global burden of ischemic heart disease (IHD) linked to ambient fine particulate matter (PM2.5) pollution from 1990 to 2021, with projections extending to 2072. Using data from the Global Burden of Disease 2021, the study reveals that middle-income countries, men, and older adults are disproportionately affected.

The editorial emphasizes the growing recognition of PM2.5 as a major cardiovascular risk factor—its impact by 2025 is expected to rival that of smoking. It revisits foundational research, including the Harvard Six Cities Study and subsequent influential publications, which established the link between air pollution and heart disease.

Key sources of PM2.5 include vehicle emissions, industrial activity, fossil fuel combustion, agriculture, household pollutants, and natural events—most of which are shaped by human behavior and policy. The editorial calls for urgent action to reduce both outdoor and indoor air pollution, integrate pollution-related cardiovascular risks into medical education, and push policymakers to address not only domestic but also cross-border pollution threats.

这篇社论强调了Enyo Tong及其同事发表在《动脉粥样硬化》杂志上的一项突破性研究，该研究调查了1990年至2021年期间与环境细颗粒物（PM2.5）污染相关的缺血性心脏病（IHD）的全球负担，并预测将持续到2072年。该研究利用《2021年全球疾病负担》的数据显示，中等收入国家、男性和老年人受到的影响不成比例。这篇社论强调，人们越来越认识到PM2.5是一个主要的心血管风险因素，预计到2025年，它的影响将与吸烟相媲美。它回顾了基础研究，包括哈佛六城研究和随后的有影响力的出版物，这些研究确立了空气污染和心脏病之间的联系。PM2.5的主要来源包括车辆排放、工业活动、化石燃料燃烧、农业、家庭污染物和自然事件——其中大部分是由人类行为和政策决定的。这篇社论呼吁采取紧急行动，减少室外和室内空气污染，将与污染有关的心血管风险纳入医学教育，并推动政策制定者不仅应对国内污染威胁，而且应对跨境污染威胁。

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引用次数: 0

Triglyceride-rich lipoproteins, remnants and atherosclerotic cardiovascular disease: What we know and what we need to know 富甘油三酯脂蛋白、残余物和动脉粥样硬化性心血管疾病：我们所知道的和我们需要知道的

IF 5.7 2区医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS

Atherosclerosis

Pub Date : 2025-11-01 DOI: 10.1016/j.atherosclerosis.2025.120529

M. John Chapman , Chris J. Packard , Elias Björnson , Henry N. Ginsberg , Jan Borén

Apolipoprotein B-containing triglyceride-rich lipoproteins (TRLs) -chylomicrons, very low-density lipoproteins (VLDL), their remnants, and intermediate-density lipoproteins (IDL) - are recognised as key contributors to atherosclerotic cardiovascular disease (ASCVD). On a per particle basis, genetic and clinical evidence indicates that TRL/remnants exhibit a greater atherogenic potential than LDL and evidence points to this being mediated by enhanced arterial wall retention of TRLs, the pro-inflammatory actions of their constituent apolipoproteins and cargo of cholesterol and bioactive lipids, and their capacity to induce endothelial dysfunction. Despite the strong association between plasma triglyceride levels and ASCVD, TRL-lowering trials have produced inconsistent, often negative results. The answer to this conundrum, as explored here, likely lies in the complexity of TRL structure, composition and metabolism, and in the dynamic influence that TRLs have on the properties of LDL, the most abundant atherogenic lipoprotein. The substantial heterogeneity in the TRL/remnant/IDL spectrum means that these particles present a wide range of potentially pathogenic factors to the artery wall in the form of major and minor lipids and a variety of surface apolipoproteins. Significant gaps exist in our knowledge: how are TRL remodelled during their lifetime in the bloodstream to become cholesterol-enriched lipoproteins; which are the most relevant TRL subspecies or TRL constituents, that initiate and progress the formation of atherosclerotic lesions; and what are the prime targets for effective intervention. Critical to the design of future triglyceride-lowering prevention trials will be the development of superior biomarkers of TRL/remnant atherogenicity and the development of a precision medicine approach to ASCVD prevention.

载脂蛋白b富含甘油三酯的脂蛋白(trl) -乳糜微粒、极低密度脂蛋白（VLDL）及其残余物和中密度脂蛋白(IDL) -被认为是动脉粥样硬化性心血管疾病（ASCVD）的关键因素。在每个颗粒的基础上，遗传和临床证据表明TRL/残留物比LDL表现出更大的动脉粥样硬化潜力，证据表明这是由TRL的动脉壁保留增强、其组成载脂蛋白和胆固醇和生物活性脂质的促炎作用以及它们诱导内皮功能障碍的能力介导的。尽管血浆甘油三酯水平与ASCVD之间存在很强的相关性，但降低trl的试验产生了不一致的，通常是阴性的结果。正如本文所探讨的，这个难题的答案可能在于TRL结构、组成和代谢的复杂性，以及TRL对LDL（最丰富的致动脉粥样硬化脂蛋白）特性的动态影响。TRL/残体/IDL光谱的巨大异质性意味着这些颗粒以主要和次要脂质以及各种表面载脂蛋白的形式对动脉壁存在广泛的潜在致病因素。在我们的知识中存在着重大的空白：TRL在血液中的一生中是如何重塑成为富含胆固醇的脂蛋白的；哪些是最相关的TRL亚种或TRL成分，启动和推进动脉粥样硬化病变的形成；有效干预的主要目标是什么。设计未来甘油三酯降低预防试验的关键将是开发TRL/残余动脉粥样硬化性的优越生物标志物和开发ASCVD预防的精准医学方法。

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引用次数: 0

Residual cardiovascular risk in CKD: Reevaluating remnant cholesterol and inflammation CKD的剩余心血管风险：重新评估残余胆固醇和炎症。

IF 5.7 2区医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS

Atherosclerosis

Pub Date : 2025-11-01 DOI: 10.1016/j.atherosclerosis.2025.120453

Haiting Huang, Guirong Dong

引用次数: 0

Sex Differences and similarities in the Management of Familial Hypercholesterolemia during life course: learning from the younglings 一生中家族性高胆固醇血症管理的性别差异和相似性：从年轻人的学习。

IF 5.7 2区医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS

Atherosclerosis

Pub Date : 2025-11-01 DOI: 10.1016/j.atherosclerosis.2025.120518

Mariko Harada-Shiba MD, PhD , Raul D. Santos MD, PhD, MSc

引用次数: 0

Exploring the causal biological association between mitochondrial genes and carotid plaques: A multiomics Mendelian randomization study. 探索线粒体基因与颈动脉斑块之间的因果生物学关联：一项多组学孟德尔随机研究。

IF 5.7 2区医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS

Atherosclerosis

Pub Date : 2025-11-01 DOI: 10.1016/j.atherosclerosis.2025.120570

Zhuyuan Yu, Xiangyuan Meng, Ziyu Zong, Qi Song, Yingchao Huo, Hao Chen

Background: To investigate the causal relationship between mitochondrial genes and the pathogenesis of carotid plaque (CP), a multiomics-integrated Mendelian randomization (MR) analysis was performed in this study.

Methods: Leveraging data from the McRae study, UK Biobank, eQTLGen Consortium, and decode database, we extracted mitochondrial gene QTLs at methylation, gene expression, and protein abundance levels as instrumental variables for MR and summary data-based Mendelian randomization (SMR) analyses. Multiomics evidence was classified by integrating MR, SMR, and colocalization results to investigate associations between mitochondria-related genes and CP.

Results: Integration of multiomics data across mQTL, eQTL, and pQTL levels revealed 16 genes (GATM, CBR4, PGS1, PTPMT1, SDSL, SLC25A28, SPRYD4, TARS2, ACAT1, GRHPR, METAP1D, NIT2, ACSM2A, AGXT, TOP1MT, and CKMT2) that passed MR and SMR analyses. Among these, GATM demonstrated Tier 1 evidence, showing consistent causal associations with CP across all three levels. Specifically, methylation of cg10760299 in GATM was associated with lower GATM expression, increased protein levels, and a greater risk of CP. However, mtDNA copy number was not significantly associated with CP risk according to MR analysis.

Conclusion: This study identifies 16 mitochondrial genes with multiomics evidence linked to CP pathogenesis across genetic, methylation, and protein levels, highlighting the potential role of mitochondrial dysfunction in CP development and the potential of mitochondrial genes as biomarkers and therapeutic targets.

背景：为了研究线粒体基因与颈动脉斑块（CP）发病机制之间的因果关系，本研究进行了多组学综合孟德尔随机化（MR）分析。方法：利用McRae研究、UK Biobank、eQTLGen Consortium和decode数据库的数据，我们提取了甲基化、基因表达和蛋白质丰度水平的线粒体基因qtl，作为MR和基于汇总数据的孟德尔随机化（SMR）分析的工具变量。结果：对mQTL、eQTL和pQTL水平的多组学数据进行整合，发现16个基因（GATM、CBR4、PGS1、PTPMT1、SDSL、SLC25A28、SPRYD4、TARS2、ACAT1、GRHPR、METAP1D、NIT2、ACSM2A、AGXT、TOP1MT和CKMT2）通过MR和SMR分析。其中，GATM显示了一级证据，在所有三个水平上显示了与CP一致的因果关系。具体来说，GATM中cg10760299的甲基化与GATM低表达、蛋白水平升高和CP风险增加相关。然而，MR分析显示mtDNA拷贝数与CP风险无显著相关性。结论：本研究通过多组学证据确定了16个线粒体基因，这些基因在遗传、甲基化和蛋白质水平上与CP发病机制有关，突出了线粒体功能障碍在CP发病中的潜在作用，以及线粒体基因作为生物标志物和治疗靶点的潜力。

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引用次数: 0