Atherosclerosis最新文献_第6页

Corrigendum to “Rising to the challenge of cardio-renal-metabolic disease in the 21st century: Translating evidence into best clinical practice to prevent and manage atherosclerosis” [Atherosclerosis, Vol 396, (September 2024), 118528] 更正："迎接 21 世纪心肾代谢疾病的挑战：将证据转化为预防和控制动脉粥样硬化的最佳临床实践"[《动脉粥样硬化》，第 396 卷，（2024 年 9 月），第 118528 页]。

IF 4.9 2区医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS

Atherosclerosis

Pub Date : 2024-11-01 DOI: 10.1016/j.atherosclerosis.2024.118610

International Cardiometabolic Working Group, Andrew Krentz , Stephan Jacob , Christian Heiss , Naveed Sattar , Soo Lim , Kamlesh Khunti , Robert H. Eckel

引用次数: 0

Progression of coronary artery calcium density and major adverse cardiovascular events 冠状动脉钙密度的进展与主要不良心血管事件。

IF 4.9 2区医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS

Atherosclerosis

Pub Date : 2024-11-01 DOI: 10.1016/j.atherosclerosis.2024.118593

Qingchao Meng, Li Zhao, Na Zhao, Yunqiang An, Bin Lu , Yang Gao

Background and aims

We aimed to investigate the relationship between coronary artery calcium (CAC) density progression and major adverse cardiovascular events (MACE), and the prognostic value of CAC density progression.

Methods

Patients with serial CAC scans were enrolled in this study. CAC density was directly measured in calcified lesions. Change and rate of progression of CAC density were calculated. Cox proportional hazard regression was utilized to estimate hazard ratios (HRs) for time to MACE regarding CAC density. The incremental prognostic value and the reclassification ability of CAC density progression were evaluated using the C-index and continuous net reclassification index (NRI).

Results

304 patients (57.86 ± 9.47 years, 69.4 % male) were included. There were 47 MACE over a follow–up period of 76.00 (56.00–95.00) months. After adjustment for risk factors and CAC volume, the change of CAC density was inversely associated with MACE (per 10HU: HR: 0.956, 95 % confidence interval: 0.920–0.992, p = 0.018). Adding the change of CAC density to risk factors and baseline CAC density improved the C-index (0.694 vs. 0.678, p = 0.026). Adding the change of CAC density improved reclassification of MACE compared with risk factors and baseline CAC density [NRI = 0.432 (0.016–0.789)].

Conclusions

CAC density progression is inversely associated with MACE. The addition of the change of CAC density improves prognostic value compared to baseline risk factors and CAC density and optimizes risk reclassification.

背景与目的我们旨在研究冠状动脉钙化（CAC）密度进展与主要不良心血管事件（MACE）之间的关系，以及CAC密度进展的预后价值：本研究招募了接受连续 CAC 扫描的患者。方法：本研究招募了接受连续 CAC 扫描的患者，直接测量钙化病灶的 CAC 密度。计算CAC密度的变化和进展率。利用 Cox 比例危险回归估算出 CAC 密度与 MACE 发生时间的危险比 (HRs)。使用C指数和连续净再分类指数（NRI）评估了CAC密度进展的增量预后价值和再分类能力：共纳入 304 名患者（57.86 ± 9.47 岁，69.4% 为男性）。在76.00（56.00-95.00）个月的随访期间，共有47例MACE。在对风险因素和 CAC 容量进行调整后，CAC 密度的变化与 MACE 呈反比（每 10HU HR：0.956，95 % 置信区间：0.920-0.992，p = 0.018）。在风险因素和基线 CAC 密度的基础上增加 CAC 密度的变化，可改善 C 指数（0.694 vs. 0.678，p = 0.026）。与危险因素和基线CAC密度相比，增加CAC密度变化可改善MACE的再分类[NRI = 0.432 (0.016-0.789)] ：结论：CAC密度的增加与MACE成反比。结论：CAC密度的变化与MACE成反比。与基线风险因素和CAC密度相比，CAC密度的变化提高了预后价值，并优化了风险再分类。

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引用次数: 0

The dual role of lipids in chronic kidney disease: Pathogenic culprits and therapeutic allies 血脂在慢性肾病中的双重作用：致病元凶与治疗盟友。

IF 4.9 2区医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS

Atherosclerosis

Pub Date : 2024-11-01 DOI: 10.1016/j.atherosclerosis.2024.118615

Elena Giardini , Dean Moore , Denise Sadlier , Catherine Godson , Eoin Brennan

Chronic kidney disease (CKD) is a significant health burden, with rising incidence and prevalence, attributed in part to increasing obesity and diabetes rates. Lipid accumulation in the kidney parenchyma and chronic, low-grade inflammation are believed to significantly contribute to the development and progression of CKD. The effect of dysregulated kidney lipid metabolism in CKD progression, including altered cholesterol and fatty acid metabolism contribute to glomerular and tubular cell injury through the activation of oxidative stress and inflammatory signalling cascades. In contrast, classes of endogenous specialized pro-resolving lipid mediators (SPMs) have been described that act to limit the inflammatory response and promote the resolution of inflammation. This review highlights our current understanding of how lipids can cause damage within the kidney, and classes of protective lipid metabolites that offer therapeutic benefits.

慢性肾脏病（CKD）是一种严重的健康负担，其发病率和流行率不断上升，部分原因是肥胖和糖尿病发病率不断增加。肾脏实质中的脂质积累和慢性低度炎症被认为是导致慢性肾脏病发生和发展的重要原因。在慢性肾功能衰竭进展过程中，肾脏脂质代谢失调的影响，包括胆固醇和脂肪酸代谢的改变，通过激活氧化应激和炎症信号级联，导致肾小球和肾小管细胞损伤。与此形成鲜明对比的是，内源性特异性促进炎症消解脂质介质（SPMs）的作用是限制炎症反应和促进炎症消解。本综述重点介绍了我们目前对脂质如何在肾脏内造成损害的认识，以及具有治疗作用的保护性脂质代谢物类别。

引用次数: 0

Metabolites derived from radical oxidation of PUFA: NEO-PUFAs, promising molecules for health? 由 PUFA 自由基氧化产生的代谢物：NEO-PUFAs，有望促进健康的分子？

IF 4.9 2区医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS

Atherosclerosis

Pub Date : 2024-11-01 DOI: 10.1016/j.atherosclerosis.2024.118600

Anna Abramova , Jamie Bride , Camille Oger , Marie Demion , Jean-Marie Galano , Thierry Durand , Jérôme Roy

Oxidative stress plays a critical role in numerous pathological processes. Under these stress conditions, the free radical-catalyzed lipid peroxidation generates in vivo a large number of key products that are involved in many physiological and pathophysiological processes. Among these products are neuroprostanes, which arise from the peroxidation of docosahexaenoic acid (DHA), and isoprostanes, resulting from arachidonic acid (AA) and eicosapentaenoic acid (EPA) through the same peroxidation process. These non-enzymatic oxygenated metabolites newly appointed NEO-PUFAs have gained recognition as reliable markers of oxidative stress in neurogenerative and cardiovascular diseases. Moreover, some of them display a wide range of biological activities. The ability to detect and measure these metabolites offers precious insights into the mechanisms of oxidative damage and holds potential therapeutic implications for various health conditions, including neurodegenerative diseases. This review focuses on the role of neuroprostanes as biomarkers for oxidative stress and related diseases, highlighting their potential applications in medical research and treatment.

氧化应激在许多病理过程中起着至关重要的作用。在这些应激条件下，自由基催化的脂质过氧化反应会在体内产生大量参与许多生理和病理生理过程的关键产物。这些产物包括由二十二碳六烯酸（DHA）过氧化反应产生的神经前列素，以及由花生四烯酸（AA）和二十碳五烯酸（EPA）通过相同的过氧化反应过程产生的异前列素。这些新命名为 NEO-PUFAs 的非酶含氧代谢物已被公认为神经退行性疾病和心血管疾病中氧化应激的可靠标志物。此外，其中一些还具有广泛的生物活性。检测和测量这些代谢物的能力为了解氧化损伤的机制提供了宝贵的视角，并对包括神经退行性疾病在内的各种健康状况具有潜在的治疗意义。这篇综述重点探讨了神经前列素作为氧化应激和相关疾病生物标记物的作用，强调了它们在医学研究和治疗中的潜在应用。

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引用次数: 0

Nucleic acid liquid biopsies in cardiovascular disease: Cell-free DNA liquid biopsies in cardiovascular disease 心血管疾病中的核酸液体活检：心血管疾病中的无细胞 DNA 液体活检。

IF 4.9 2区医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS

Atherosclerosis

Pub Date : 2024-11-01 DOI: 10.1016/j.atherosclerosis.2024.118583

Tyler Artner, Smriti Sharma, Irene M. Lang

Cardiovascular disease (CVD) is the leading cause of death worldwide, and despite treatment efforts, cardiovascular function cannot always be restored, and progression of disease be prevented. Critical insights are oftentimes based on tissue samples. Current knowledge of tissue pathology typically relies on invasive biopsies or postmortem samples. Liquid biopsies, which assess circulating mediators to deduce the histology and pathology of distant tissues, have been advancing rapidly in cancer research and offer a promising approach to be translated to the understanding and treatment of CVD. The widely understood elevations in cell-free DNA during acute and chronic cardiovascular conditions, associate with disease, severity, and offer prognostic value. The role of neutrophil extracellular traps (NETs) and circulating nucleases in thrombosis provide a solid rationale for liquid biopsies in CVD. cfDNA originates from various tissue types and cellular sources, including mitochondria and nuclei, and can be used to trace cell and tissue type lineage, as well as to gain insight into the activation status of cells. This article discusses the origin, structure, and potential utility of cfDNA, offering a deeper and less invasive approach for the understanding of the complexities of CVD.

心血管疾病（CVD）是导致全球死亡的主要原因，尽管已经进行了治疗，但心血管功能并不总能恢复，疾病的恶化也无法预防。关键的见解往往基于组织样本。目前的组织病理学知识通常依赖于侵入性活检或死后样本。液体活检通过评估循环介质来推断远处组织的组织学和病理学，在癌症研究领域进展迅速，为了解和治疗心血管疾病提供了一种前景广阔的方法。众所周知，在急性和慢性心血管疾病期间，游离细胞 DNA 的升高与疾病、严重程度有关，并具有预后价值。中性粒细胞胞外捕获物（NET）和循环核酸酶在血栓形成中的作用为在心血管疾病中进行液体活检提供了可靠的依据。cfDNA 来源于不同的组织类型和细胞来源，包括线粒体和细胞核，可用于追踪细胞和组织类型的血统，并深入了解细胞的活化状态。本文讨论了 cfDNA 的起源、结构和潜在用途，为了解心血管疾病的复杂性提供了一种更深入、创伤更小的方法。

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引用次数: 0

Association of colchicine use with cardiovascular and limb events in peripheral artery disease: Insights from a retrospective cohort study 外周动脉疾病患者使用秋水仙碱与心血管和肢体事件的关系：一项回顾性队列研究的启示。

IF 4.9 2区医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS

Atherosclerosis

Pub Date : 2024-11-01 DOI: 10.1016/j.atherosclerosis.2024.118563

Lucas Tramujas , Alleh Nogueira , Nicole Felix , Pedro Gabriel Melo de Barros e Silva , Alexandre Abizaid , Alexandre Biasi Cavalcanti

Background and aims

Colchicine has demonstrated efficacy in treating coronary artery disease, but its efficacy in peripheral artery disease (PAD) remains uncertain. This study aims to address this gap in knowledge.

Methods

A retrospective cohort study was conducted using the TriNetX Network, selecting patients with lower limb PAD between January 1, 2011, and January 1, 2024. Colchicine users were matched 1:1 with non-users through propensity score matching, considering demographics, medical conditions, medications, and psychosocial factors. The primary outcome was a composite of major adverse cardiovascular and limb events (MACLE) - including lower limb amputation, revascularization for lower limb ischemia, acute myocardial infarction, ischemic stroke, and all-cause mortality – over a ten-year follow-up.

Results

From 53,568 colchicine-treated and 1,499,969 untreated patients with lower limb PAD, 52,350 pairs were successfully matched. Over ten years, colchicine was associated with a significant reduction in MACLE (hazard ratio, [HR] 0.90, 95% CI 0.88–0.92, p < 0.001), any lower limb amputation (HR 0.84, 95% CI 0.75–0.94, p = 0.002), revascularization for lower limb ischemia (HR 0.85, 95% CI 0.82–0.88, p < 0.001), major adverse cardiovascular events (HR 0.93, 95% CI 0.91–0.95, p < 0.001), and all-cause mortality (HR 0.90, 95% CI 0.87–0.92, p < 0.001). It also result in a reduced risk of ischemic stroke (HR 0.95, 95% CI 0.92–0.98, p = 0.001), but not of acute myocardial infarction (HR 0.98, 95% CI 0.95–1.01, p = 0.24).

Conclusions

Colchicine significantly reduced major adverse cardiovascular and limb events in patients with lower limb PAD, supporting the need for further investigation.

背景和目的：秋水仙碱在治疗冠状动脉疾病方面疗效显著，但对外周动脉疾病（PAD）的疗效仍不确定。本研究旨在填补这一知识空白：利用 TriNetX 网络进行了一项回顾性队列研究，选择了 2011 年 1 月 1 日至 2024 年 1 月 1 日期间的下肢 PAD 患者。考虑到人口统计学、医疗条件、药物和社会心理因素，通过倾向得分匹配法将使用秋水仙碱的患者与未使用秋水仙碱的患者进行1:1配对。主要结果是十年随访期间主要心血管和肢体不良事件（MACLE）的综合结果，包括下肢截肢、下肢缺血血管重建、急性心肌梗死、缺血性中风和全因死亡率：在53,568名接受过秋水仙碱治疗和1,499,969名未接受过治疗的下肢PAD患者中，有52,350对成功配对。十年间，秋水仙碱与 MACLE 的显著减少有关（危险比 [HR] 0.90，95% CI 0.88-0.92，P 结论）：秋水仙碱能明显减少下肢PAD患者的主要心血管和肢体不良事件，因此有必要进行进一步研究。

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引用次数: 0

Readmission outcomes after acute coronary syndrome among patients with myeloproliferative neoplasms. 骨髓增生性肿瘤患者急性冠状动脉综合征后再入院的结果。

IF 4.9 2区医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS

Atherosclerosis

Pub Date : 2024-11-01 DOI: 10.1016/j.atherosclerosis.2024.119046

Orly Leiva, Sophia Zhou, Joan How, Michelle Lee, Gabriela Hobbs

Background and aims: Myeloproliferative neoplasms (MPNs) are associated with arterial thrombosis, including acute coronary syndrome (ACS). Prior studies have suggested similar in-hospital mortality among patients with MPN compared to those without. However, post-ACS outcomes have not been thoroughly evaluated.

Methods: Patients hospitalized for ACS with and without MPN from January 2014 to December 2020 were identified using the National Readmission Database (NRD). Primary outcome was 90- and 180-day cardiovascular (CV) readmissions. Secondary outcomes were 90- and 180-day arterial thrombosis (AT), heart failure (HF), bleeding, and all-cause readmission and index hospitalization death, bleeding and arterial thrombosis (including ischemic stroke and arterial thromboembolism). Propensity score matching was used to compare outcomes between patients with and without MPN.

Results: After PSM, 8667 patients with MPN were matched with 43,335 patients without MPN. MPN was associated with increased risk of 90- (HR 1.22, 95 % CI 1.13-1.32) and 180-day (HR 1.22, 95 % CI 1.12-1.32) readmissions. MPN was also associated with increased risk of 90- and 180-day AT, HF, bleeding, and all-cause readmissions. Among patients with MPN, MF was associated with increased risk of 90- (HR 1.36, 95 % CI 1.24-1.50) and 180- day (HR 1.34, 95 % CI 1.21-1.48) readmissions.

Conclusions: MPN was associated with increased risk of 90- and 180-day readmissions among patients hospitalized for ACS. Among patients with MPN, MF was associated with increased risk of 90- and 180-day CV readmissions. Further investigation is needed to improve post-ACS outcomes among patients with MPN.

背景和目的：骨髓增生性肿瘤（mpn）与动脉血栓形成有关，包括急性冠状动脉综合征（ACS）。先前的研究表明，与没有MPN的患者相比，MPN患者的住院死亡率相似。然而，acs后的结果尚未得到彻底评估。方法：使用国家再入院数据库（NRD）对2014年1月至2020年12月住院的伴有或不伴有MPN的ACS患者进行识别。主要终点是90天和180天的心血管（CV）再入院。次要结局为90天和180天动脉血栓形成（AT）、心力衰竭（HF）、出血、全因再入院和指数住院死亡、出血和动脉血栓形成（包括缺血性卒中和动脉血栓栓塞）。倾向评分匹配用于比较有和没有MPN的患者之间的结果。结果：经PSM后，8667例MPN患者与43335例无MPN患者配对。MPN与90天（HR 1.22, 95% CI 1.13-1.32）和180天（HR 1.22, 95% CI 1.12-1.32）再入院风险增加相关。MPN还与90天和180天AT、HF、出血和全因再入院的风险增加有关。在MPN患者中，MF与90天（HR 1.36, 95% CI 1.24-1.50）和180天（HR 1.34, 95% CI 1.21-1.48）再入院风险增加相关。结论：在因ACS住院的患者中，MPN与90天和180天再入院风险增加相关。在MPN患者中，MF与90天和180天CV再入院风险增加相关。需要进一步的研究来改善MPN患者acs后的预后。

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引用次数: 0

Role of fatty acids in the pathogenesis of ß-cell failure and Type-2 diabetes 脂肪酸在 ß 细胞衰竭和 2 型糖尿病发病机制中的作用。

IF 4.9 2区医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS

Atherosclerosis

Pub Date : 2024-11-01 DOI: 10.1016/j.atherosclerosis.2024.118623

Cecilia Jiménez-Sánchez, Lucie Oberhauser, Pierre Maechler

Pancreatic ß-cells are glucose sensors in charge of regulated insulin delivery to the organism, achieving glucose homeostasis and overall energy storage. The latter function promotes obesity when nutrient intake chronically exceeds daily expenditure. In case of ß-cell failure, such weight gain may pave the way for the development of Type-2 diabetes. However, the causal link between excessive body fat mass and potential degradation of ß-cells remains largely unknown and debated. Over the last decades, intensive research has been conducted on the role of lipids in the pathogenesis of ß-cells, also referred to as lipotoxicity. Among various lipid species, the usual suspects are essentially the non-esterified fatty acids (NEFA), in particular the saturated ones such as palmitate. This review describes the fundamentals and the latest advances of research on the role of fatty acids in ß-cells. This includes intracellular pathways and receptor-mediated signaling, both participating in regulated glucose-stimulated insulin secretion as well as being implicated in ß-cell dysfunction. The discussion extends to the contribution of high glucose exposure, or glucotoxicity, to ß-cell defects. Combining glucotoxicity and lipotoxicity results in the synergistic and more deleterious glucolipotoxicity effect. In recent years, alternative roles for intracellular lipids have been uncovered, pointing to a protective function in case of nutrient overload. This requires dynamic storage of NEFA as neutral lipid droplets within the ß-cell, along with active glycerolipid/NEFA cycle allowing subsequent recruitment of lipid species supporting glucose-stimulated insulin secretion. Overall, the latest studies have revealed the two faces of the same coin.

胰腺ß-细胞是葡萄糖传感器，负责向机体输送胰岛素，实现葡萄糖平衡和总体能量储存。当营养摄入长期超过每日消耗时，胰腺ß细胞的后一种功能会导致肥胖。如果ß细胞功能失效，体重增加可能会为发展成2型糖尿病铺平道路。然而，过多的体内脂肪量与ß细胞的潜在退化之间的因果关系在很大程度上仍不为人所知，也存在争议。过去几十年来，人们一直在深入研究脂质在ß细胞发病机制中的作用，这也被称为脂毒性。在各种脂质中，最常见的是非酯化脂肪酸（NEFA），尤其是饱和脂肪酸，如棕榈酸酯。本综述介绍了脂肪酸在ß细胞中作用的基本原理和最新研究进展。这包括细胞内途径和受体介导的信号传导，两者都参与调节葡萄糖刺激的胰岛素分泌，并与ß细胞功能障碍有关。讨论延伸到高葡萄糖暴露或葡萄糖毒性对ß细胞缺陷的影响。将葡萄糖毒性和脂肪毒性结合在一起，会产生协同作用和更具破坏性的葡萄糖脂肪毒性效应。近年来，人们发现了细胞内脂质的另一种作用，即在营养过剩的情况下发挥保护功能。这就需要在ß细胞内以中性脂滴的形式动态储存 NEFA，同时进行活跃的甘油脂/NEFA 循环，以便随后招募脂质物种支持葡萄糖刺激的胰岛素分泌。总之，最新研究揭示了同一枚硬币的两面。

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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 : 2024-11-01 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

HMGB2 promotes smooth muscle cell proliferation through PPAR-γ/PGC-1α pathway-mediated glucose changes in aortic dissection 在主动脉夹层中，HMGB2 通过 PPAR-γ/PGC-1α 通路介导的葡萄糖变化促进平滑肌细胞增殖。

IF 4.9 2区医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS

Atherosclerosis

Pub Date : 2024-10-31 DOI: 10.1016/j.atherosclerosis.2024.119044

Yameng Zheng , Mengge Yao , Shaokun Chen , Jiakang Li , Xiaozhen Wei , Zhihuang Qiu , Liangwan Chen , Li Zhang

Background and aims

Aortic dissection (AD) is a fatal condition with a complicated pathogenesis. High mobility group protein B2 (HMGB2) is a member of the high mobility group protein family; HMGB2 is involved in innate immunity and inflammatory diseases, but its role in AD remains unclear.

Methods

HMGB2^−/− mice were generated and treated with β-aminopropionitrile and angiotensin II (Ang II) to establish an AD model. An F12 gel containing AAV9-HMGB2 was applied to overexpress HMGB2 in mice. Pathological changes in the aorta were assessed by visualizing vascular collagen deposition and elastic fiber fracture via H&E, Masson and EVG staining. HMGB2 expression was measured by Western blotting and immunohistochemistry. MTS, CCK-8 and EdU assays were used to test cell proliferation.

Results

HMGB2 expression was increased in samples from AD patients, samples from AD mouse modeland human aortic smooth muscle cells (HASMCs). HMGB2 promoted HASMC proliferation. Immunofluorescence staining and plasma membrane protein isolation revealed that HMGB2 decreased GLUT1 expression and promoted GLUT4 translocation. HMGB2 was also found to inhibit the expression of SIRT1/PGC-1α, but blocking the PPAR-γ pathway attenuated this effect. HMGB2^−/− significantly reduced the incidence and mortality rates of AD, whereas treatment with AAV9-HMGB2 exacerbated AD.

Conclusions

This study suggests that HMGB2 promotes HASMC proliferation and vascular remodeling by regulating glucose metabolism through the PPAR-γ/SIRT1/PGC-1α pathway. HMGB2 knockdown reduces, while HMGB2 overexpression promotes, the occurrence of AD in mice. This study may help elucidate the underlying mechanisms and provide a new preventive target for AD.

背景和目的：主动脉夹层（AD）是一种致命疾病，发病机制复杂。高迁移率基团蛋白 B2（HMGB2）是高迁移率基团蛋白家族的成员；HMGB2 参与先天性免疫和炎症性疾病，但其在 AD 中的作用仍不清楚。方法：产生 HMGB2-/-小鼠，并用 β-氨基丙腈和血管紧张素 II（Ang II）处理，以建立 AD 模型。应用含有 AAV9-HMGB2 的 F12 凝胶在小鼠体内过表达 HMGB2。通过H&E、Masson和EVG染色观察血管胶原沉积和弹性纤维断裂，评估主动脉的病理变化。通过 Western 印迹和免疫组化检测 HMGB2 的表达。采用 MTS、CCK-8 和 EdU 检测法检测细胞增殖：结果：AD 患者样本、AD 小鼠模型样本和人主动脉平滑肌细胞（HASMCs）中 HMGB2 的表达均有所增加。HMGB2 促进了 HASMC 的增殖。免疫荧光染色和质膜蛋白分离显示，HMGB2 降低了 GLUT1 的表达并促进了 GLUT4 的转位。研究还发现，HMGB2 可抑制 SIRT1/PGC-1α 的表达，但阻断 PPAR-γ 通路可减轻这种影响。HMGB2-/-能显著降低AD的发病率和死亡率，而用AAV9-HMGB2治疗则会加重AD：本研究表明，HMGB2 通过 PPAR-γ/SIRT1/PGC-1α 途径调节葡萄糖代谢，从而促进 HASMC 增殖和血管重塑。敲除 HMGB2 可减少小鼠 AD 的发生，而过表达 HMGB2 则会促进 AD 的发生。这项研究可能有助于阐明其潜在机制，并为AD提供一个新的预防靶点。

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引用次数: 0