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The Role of Circular RNA in the Pathogenesis of Chemotherapy-Induced Cardiotoxicity in Cancer Patients: Focus on the Pathogenesis and Future Perspective. 环状 RNA 在癌症患者化疗诱发心脏毒性发病机制中的作用:聚焦发病机制与未来展望》。
IF 3.4 3区 医学 Q2 CARDIAC & CARDIOVASCULAR SYSTEMS Pub Date : 2024-11-01 Epub Date: 2024-08-19 DOI: 10.1007/s12012-024-09914-w
Pegah Joghataie, Mahya Bakhshi Ardakani, Neda Sabernia, Afshin Salary, Sepehr Khorram, Tooba Sohbatzadeh, Vahid Goodarzi, Bahareh Shateri Amiri

Cardiotoxicity is a serious challenge cancer patients face today. Various factors are involved in cardiotoxicity. Circular RNAs (circRNAs) are one of the effective factors in the occurrence and prevention of cardiotoxicity. circRNAs can lead to increased proliferation, apoptosis, and regeneration of cardiomyocytes by regulating the molecular pathways, as well as increasing or decreasing gene expression; some circRNAs have a dual role in cardiomyocyte regeneration or death. Identifying each of the pathways related to these processes can be effective on managing patients and preventing cardiotoxicity. In this study, an overview of the molecular pathways involved in cardiotoxicity by circRNAs and their effects on the downstream factors have been discussed.

心脏毒性是当今癌症患者面临的一项严峻挑战。心脏毒性涉及多种因素。环状核糖核酸(circRNA)是发生和预防心脏毒性的有效因素之一。环状核糖核酸可通过调节分子通路以及增加或减少基因表达,导致心肌细胞增殖、凋亡和再生;有些环状核糖核酸在心肌细胞再生或死亡中具有双重作用。确定与这些过程相关的每种途径可有效控制患者病情并预防心脏毒性。本研究概述了 circRNAs 参与心脏毒性的分子通路及其对下游因子的影响。
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引用次数: 0
Vascular Stress Markers Following Inhalation of Heated Tobacco Products: A Study on Extracellular Vesicles. 吸入加热烟草制品后的血管应激标志物:细胞外囊泡研究。
IF 3.4 3区 医学 Q2 CARDIAC & CARDIOVASCULAR SYSTEMS Pub Date : 2024-10-29 DOI: 10.1007/s12012-024-09934-6
Lukasz Antoniewicz, Georgy Melnikov, Gustaf Lyytinen, Anders Blomberg, Jenny A Bosson, Linnea Hedman, Fariborz Mobarrez, Magnus Lundbäck

The advent of heated tobacco products (HTPs) has introduced new variables in the study of nicotine delivery systems and their health implications. Amidst concerns over cardiovascular effects, this study aims to elucidate the acute impact of HTP inhalation on extracellular vesicles (EV) levels in young, healthy individuals. In this controlled, acute exposure study, 23 young, healthy volunteers were subjected to HTP inhalation. EV levels of endothelial and platelet origin were quantified through flow cytometry before and after exposure. Data analysis was performed using multiple measures ANOVA to assess changes in EV concentrations. Our findings reveal a significant increase in EVs of endothelial and platelet origin following short-term HTP inhalation with nicotine. Notably, no significant change was observed in leukocyte- and neutrophil-derived EVs. This increase in EVs suggests acute vascular stress, with peak levels observed 4 h post-exposure. The rise in endothelial and platelet-derived EVs aligns with documented responses to acute vascular injury, paralleling the effects seen with traditional cigarette and e-cigarette use. Despite HTPs being marketed as safer alternatives, our results indicate that nicotine-containing HTPs may still pose significant vascular risks. These findings contribute to the growing body of evidence cautioning against the perceived safety of HTPs and reinforce the importance of regulatory oversight and public health initiatives targeting nicotine delivery technologies. Trial Registrations: ClinicalTrials.gov ID: NCT04824495, registered 2021-01-07.

加热烟草制品(HTPs)的出现为尼古丁给药系统及其健康影响的研究引入了新的变量。鉴于人们对心血管影响的担忧,本研究旨在阐明吸入加热烟草制品对年轻健康人细胞外小泡(EV)水平的急性影响。在这项受控急性暴露研究中,23 名年轻健康的志愿者吸入了 HTP。在接触前后,通过流式细胞术对内皮和血小板来源的 EV 水平进行了量化。数据分析采用多元方差分析来评估 EV 浓度的变化。我们的研究结果表明,短期吸入尼古丁的 HTP 后,内皮和血小板来源的 EV 明显增加。值得注意的是,白细胞和中性粒细胞来源的 EVs 没有明显变化。EVs 的增加表明存在急性血管应激,在暴露后 4 小时达到峰值。内皮和血小板衍生 EVs 的增加与文献记载的对急性血管损伤的反应一致,与传统香烟和电子烟的影响相似。尽管 HTP 在市场上被当作更安全的替代品,但我们的研究结果表明,含有尼古丁的 HTP 仍可能对血管构成重大风险。这些发现为越来越多的证据提供了依据,告诫人们不要认为 HTPs 是安全的,并强化了针对尼古丁递送技术的监管监督和公共卫生措施的重要性。试验注册:ClinicalTrials.gov ID:NCT04824495,注册日期为 2021-01-07。
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引用次数: 0
Inhibition of CB1R in the Hypothalamic Paraventricular Nucleus Ameliorates Hypertension Through Wnt/β-Catenin/RAS Pathway. 抑制下丘脑室旁核中的 CB1R 可通过 Wnt/β-Catenin/RAS 通路改善高血压状况
IF 3.4 3区 医学 Q2 CARDIAC & CARDIOVASCULAR SYSTEMS Pub Date : 2024-10-28 DOI: 10.1007/s12012-024-09938-2
Hong-Li Gao, Yu Yang, Hua Tian, Li-Yan Fu, Kai-Li Liu, Xiu-Yue Jia, Xiao-Lian Shi, Yu-Ming Kang, Xiao-Jing Yu

The hypothalamic paraventricular nucleus (PVN), as an important integrating center, plays a prominent role in the pathogenesis of hypertension, in maintaining the stability of cardiovascular activity through peripheral sympathetic nervous activity and secretion of various humoral factors. Acknowledging that the mechanistic targets of the endocannabinoid type 1 receptor (CB1R) are the key signaling systems involved in the regulation of hypertension, we sought to clarify whether inhibition of CB1R within the PVN ameliorates hypertension through Wnt/β-catenin/RAS pathway. Spontaneously hypertensive rats (SHRs) and Wistar Kyoto rats were randomly assigned to different groups and treated with bilateral PVN injections of AM251 (CB1R antagonist, 10 µg/h) or vehicle (artificial cerebrospinal fluid, aCSF) for four weeks. Bilateral PVN injections of AM251 significantly decreased the heart rate, the body weight and the mean arterial pressure in SHRs. AM251 lowered the expression of CB1R, Wnt3, active-β-catenin, p-IKKβ, RAS components, pro-inflammatory cytokines and elevated the expression level of Glycogen synthase kinase3β and Superoxide Dismutase in the PVN of hypertensive rats. Our findings suggest that inhibition of CB1R in the PVN ameliorates hypertension through Wnt/β-catenin/RAS pathway and broaden our current understanding of the pathological mechanism and clinical treatment of hypertension.

下丘脑室旁核(PVN)作为一个重要的整合中枢,通过外周交感神经活动和分泌各种体液因子维持心血管活动的稳定,在高血压的发病机制中发挥着突出的作用。鉴于内源性大麻素1型受体(CB1R)的机理靶点是参与调控高血压的关键信号系统,我们试图阐明抑制PVN内的CB1R是否能通过Wnt/β-catenin/RAS途径改善高血压。将自发性高血压大鼠(SHRs)和Wistar Kyoto大鼠随机分配到不同的组,双侧PVN注射AM251(CB1R拮抗剂,10 µg/h)或药物(人工脑脊液,aCSF)治疗四周。双侧皮质神经网注射 AM251 能显著降低 SHR 的心率、体重和平均动脉压。AM251 降低了高血压大鼠 PVN 中 CB1R、Wnt3、活性-β-catenin、p-IKKβ、RAS 成分、促炎细胞因子的表达,并提高了糖原合酶激酶 3β 和超氧化物歧化酶的表达水平。我们的研究结果表明,通过 Wnt/β-catenin/RAS 通路抑制 PVN 中的 CB1R 可改善高血压,这拓宽了我们目前对高血压病理机制和临床治疗的认识。
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引用次数: 0
Di-(2-ethylhexyl) Phthalate Exposure Induces Developmental Toxicity in the Mouse Fetal Heart via Mitochondrial Dysfunction. 邻苯二甲酸二(2-乙基己酯)暴露通过线粒体功能障碍诱发小鼠胎儿心脏的发育毒性
IF 3.4 3区 医学 Q2 CARDIAC & CARDIOVASCULAR SYSTEMS Pub Date : 2024-10-25 DOI: 10.1007/s12012-024-09936-4
Yafei Guo, Bowen Li, Yu Yan, Nanjun Zhang, Shuran Shao, Lixia Yang, Lixue Ouyang, Ping Wu, Fan Ma, Hongyu Duan, Kaiyu Zhou, Yimin Hua, Chuan Wang

Congenital heart disease (CHD) is a major cause of infant mortality and morbidity, with growing interest in the role of environmental factors in its etiology. Di-(2-ethylhexyl) phthalate (DEHP), an environmental endocrine disruptor, has been implicated in the development of CHD. This study aimed to investigate the effects of DEHP exposure on fetal heart development in mice. Pregnant mice exposed to DEHP exhibited increased fetal malformations, decreased fetal weight, and reduced crown-rump length.f Transcriptomic analysis revealed the downregulation of genes involved in aerobic respiration and mitochondrial ATP synthesis. Functional assays demonstrated reduced mitochondrial respiration, decreased ATP production, elevated reactive oxygen species levels, and lowered mitochondrial membrane potential in DEHP-exposed fetal cardiomyocytes. These findings underscore the detrimental effects of DEHP on fetal cardiac health and provide insights into the molecular mechanisms underlying DEHP-induced CHD. Understanding these mechanisms is crucial for developing preventive strategies against environmental toxicants that affect fetal cardiac development.

先天性心脏病(CHD)是婴儿死亡和发病的主要原因之一,人们越来越关注环境因素在其病因中的作用。邻苯二甲酸二(2-乙基己基)酯(DEHP)是一种环境内分泌干扰物,被认为与先天性心脏病的发病有关。本研究旨在调查接触 DEHP 对小鼠胎儿心脏发育的影响。转录组分析显示,参与有氧呼吸和线粒体 ATP 合成的基因下调。功能测试显示,在暴露于 DEHP 的胎儿心肌细胞中,线粒体呼吸减少,ATP 生成减少,活性氧水平升高,线粒体膜电位降低。这些发现强调了DEHP对胎儿心脏健康的有害影响,并提供了对DEHP诱发先天性心脏病的分子机制的见解。了解这些机制对于制定针对影响胎儿心脏发育的环境毒物的预防策略至关重要。
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引用次数: 0
Association of Iron Therapy with Mortality in Patients with Acute Myocardial Infarction and Iron Deficiency. 铁治疗与急性心肌梗死和缺铁患者死亡率的关系
IF 3.4 3区 医学 Q2 CARDIAC & CARDIOVASCULAR SYSTEMS Pub Date : 2024-10-01 Epub Date: 2024-08-02 DOI: 10.1007/s12012-024-09905-x
Ye Ding, Yiyan Zhang, Xin Gao, Chang Hua, Linsheng Liu, Dan Huang

Iron deficiency (ID) is common in patients with acute myocardial infarction (AMI). It is unknown whether patients with AMI combined with ID will benefit from iron supplementation therapy. This study aimed to assess the relationship between iron therapy and mortality in AMI patients. Retrospective analysis was performed in subjects screened from the Medical Information Mart in Intensive Care-IV database. The data were obtained from ICU patients admitted to Beth Israel Deaconess Medical Center between 2008 and 2019. The patients were divided into two groups according to iron treatment exposure. Propensity score matching (PSM) was performed in the original cohort at a 1:1 ratio. Univariate and multivariate analyses were performed to adjust for confounding factors. The primary outcome was 28-day mortality. A total of 426 patients were included in this study. After 1:1 PSM, 208 patients were analyzed. Iron treatment was associated with a lower risk of 28-day mortality (9 deaths (8.65%) in the iron treatment group vs. 21 deaths (20.19%) in the non-iron treatment group; HR = 0.39; 95% CI = 0.17-0.89; p = 0.025) and in-hospital mortality (4 deaths (3.85%) in the iron treatment group vs. 12 deaths (11.54%) in the non-iron treatment group; OR, 0.15; 95% CI, 0.03-0.74; p = 0.029). Iron treatment was associated with reduced 28-day mortality in patients with AMI combined with ID. Iron treatment had no significant effect on the length of hospitalization or the length of ICU stay. Prospective studies are needed to verify this conclusion.

缺铁(ID)在急性心肌梗死(AMI)患者中很常见。急性心肌梗死合并缺铁的患者是否会从补铁治疗中获益尚不清楚。本研究旨在评估铁剂治疗与急性心肌梗死患者死亡率之间的关系。研究人员对从重症监护医学信息市场-IV 数据库中筛选出的受试者进行了回顾性分析。数据来自贝斯以色列女执事医疗中心在 2008 年至 2019 年期间收治的重症监护病房患者。根据铁治疗暴露将患者分为两组。在原始队列中按1:1的比例进行倾向得分匹配(PSM)。进行了单变量和多变量分析,以调整混杂因素。主要结果是 28 天死亡率。本研究共纳入 426 名患者。在 1:1 PSM 后,对 208 名患者进行了分析。铁剂治疗与较低的 28 天死亡风险相关(铁剂治疗组有 9 人死亡(8.65%),而非铁剂治疗组有 21 人死亡(20.19%);HR = 0.39;95% CI = 0.17-0.89;P = 0.025)和院内死亡率(铁剂治疗组 4 例死亡(3.85%),非铁剂治疗组 12 例死亡(11.54%);OR,0.15;95% CI,0.03-0.74;P = 0.029)。铁剂治疗可降低急性心肌梗死合并内科疾病患者的 28 天死亡率。铁剂治疗对住院时间或重症监护室住院时间没有明显影响。需要进行前瞻性研究来验证这一结论。
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引用次数: 0
Associations Between CYP3A5 (c.6986A>G) Gene Polymorphism and Kidney Impairment in Hypertensive Adults Without Cystatin C Elevation. CYP3A5(c.6986A>G)基因多态性与无胱抑素 C 升高的高血压成人肾功能损害之间的关系
IF 3.4 3区 医学 Q2 CARDIAC & CARDIOVASCULAR SYSTEMS Pub Date : 2024-10-01 Epub Date: 2024-08-02 DOI: 10.1007/s12012-024-09902-0
Ling Chen, Yufeng Jiang, Xingbo Cheng

Objective: This study aimed to explore the potential role of CYP3A5 (c. 6986A>G) gene polymorphism in predicting kidney function impairment in patients with hypertension who did not have elevated serum cystatin C.

Methods: We recruited a group of patients with hypertension who did not have elevated cystatin C and analyzed the CYP3A5 (c. 6986A>G) gene polymorphism. Chi-square tests were used to compare the clinical characteristics and genotypic distribution between the two groups. Logistic regression analysis was used to explore the association between CYP3A5 (c.6986A>G) gene polymorphism and renal function impairment in hypertension with non-elevated cystatin.

Results: In patients with hypertension who participated in the study, there was a significant association between CYP3A5 (c. 6986A>G) gene polymorphism and kidney function impairment (p < 0.05). Patients with the CYP3A5 (c. 6986A>G) mutation display a greater risk of kidney function impairment.

Conclusion: CYP3A5 (c. 6986A>G) gene AA homozygote polymorphism significantly increases risk of kidney function impairment in patients with hypertension with normal cystatin C. However, further studies are needed to validate this association and to further understand the mechanism of CYP3A5 (c. 6986A>G) gene polymorphism in kidney function impairment in patients with hypertension.

研究目的本研究旨在探讨CYP3A5(c. 6986A>G)基因多态性在预测血清胱抑素C未升高的高血压患者肾功能损害中的潜在作用:我们招募了一组未出现胱抑素 C 升高的高血压患者,并对其 CYP3A5 (c. 6986A>G)基因多态性进行了分析。采用卡方检验比较两组患者的临床特征和基因型分布。采用逻辑回归分析探讨胱抑素不升高的高血压患者CYP3A5(c.6986A>G)基因多态性与肾功能损害之间的关系:在参与研究的高血压患者中,CYP3A5(c. 6986A>G)基因多态性与肾功能损害之间存在显著关联(p G)突变显示肾功能损害的风险更大:CYP3A5(c. 6986A>G)基因AA同源多态性会显著增加胱抑素C正常的高血压患者肾功能损害的风险。然而,还需要进一步的研究来验证这种关联,并进一步了解CYP3A5(c. 6986A>G)基因多态性在高血压患者肾功能损害中的作用机制。
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引用次数: 0
Hsa_circ_0007765 Promotes Platelet-Derived Growth Factor-BB-Induced Proliferation and Migration of Human Aortic Vascular Smooth Muscle Cells in Atherosclerosis. Hsa_circ_0007765 在动脉粥样硬化中促进血小板衍生生长因子-BB 诱导的人主动脉血管平滑肌细胞的增殖和迁移。
IF 3.4 3区 医学 Q2 CARDIAC & CARDIOVASCULAR SYSTEMS Pub Date : 2024-10-01 Epub Date: 2024-08-10 DOI: 10.1007/s12012-024-09899-6
Shengwei Ma, Haiyun Qian, Qian Zhou, Chengang Lei

Human aortic vascular smooth muscle cells (HA-VSMCs) play vital roles in the pathogenesis of vascular diseases, including Atherosclerosis (AS). Circular RNAs (circRNAs) have been reported to regulate the biological functions of HA-VSMCs. Therefore, this study aimed to explore the role and mechanism of hsa_circRNA_102353 (circ_0007765) in platelet-derived growth factor-BB (PDGF-BB)-induced HA-VSMCs. Circ_0007765, microRNA-654-3p (miR-654-3p), and Fibroblast Growth Factor Receptor Substrate 2 (FRS2) expression were measured using real-time quantitative polymerase chain reaction (RT-qPCR). Cell proliferative ability, invasion, and migration were detected by 3-(4, 5-dimethyl-2-thiazolyl)-2, 5-diphenyl-2-H-tetrazolium bromide (MTT), 5-ethynyl-2'-deoxyuridine (EdU), Transwell, and wound healing assays. CyclinD1, MMP2, and FRS2 protein levels were assessed using a Western blot assay. Binding between miR-654-3p and circ_0007765 or FRS2 was predicted by Circinteractome or TargetScan, and verified using dual-luciferase reporter and RNA pull-down assays. PDGF-BB induced HA-VSMC proliferation, invasion, and migration. Circ_0007765 and FRS2 expression levels were increased in PDGF-BB-treated HA-VSMCs, and the miR-654-3p level was reduced. Moreover, circ_0007765 absence hindered PDGF-BB-induced HA-VSMC proliferation, invasion, and migration in vitro. At the molecular level, circ_0007765 increased FRS2 expression by acting as a sponge for miR-654-3p. Our findings revealed that circ_0007765 boosted PDGF-BB-induced HA-VSMC proliferation and migration through elevating FRS2 expression via adsorbing miR-654-3p, providing a feasible therapeutic strategy for AS.

人体主动脉血管平滑肌细胞(HA-VSMCs)在动脉粥样硬化(AS)等血管疾病的发病机制中发挥着重要作用。据报道,环状 RNA(circRNA)可调控 HA-VSMC 的生物功能。因此,本研究旨在探讨 hsa_circRNA_102353 (circ_0007765) 在血小板衍生生长因子-BB(PDGF-BB)诱导的 HA-VSMCs 中的作用和机制。使用实时定量聚合酶链反应(RT-qPCR)测定了 Circ_0007765、microRNA-654-3p(miR-654-3p)和成纤维细胞生长因子受体底物 2(FRS2)的表达。细胞增殖能力、侵袭和迁移通过 3-(4,5-二甲基-2-噻唑基)-2,5-二苯基-2-H-溴化四氮唑(MTT)、5-乙炔基-2'-脱氧尿苷(EdU)、Transwell 和伤口愈合试验进行检测。采用 Western 印迹法评估 CyclinD1、MMP2 和 FRS2 蛋白水平。通过 Circinteractome 或 TargetScan 预测了 miR-654-3p 与 circ_0007765 或 FRS2 之间的结合,并通过双荧光素酶报告和 RNA 拉取试验进行了验证。PDGF-BB 可诱导 HA-VSMC 增殖、侵袭和迁移。经 PDGF-BB 处理的 HA-VSMC 中,Circ_0007765 和 FRS2 的表达水平升高,miR-654-3p 水平降低。此外,缺乏 circ_0007765 会阻碍 PDGF-BB 诱导的 HA-VSMC 体外增殖、侵袭和迁移。在分子水平上,circ_0007765 作为 miR-654-3p 的海绵,增加了 FRS2 的表达。我们的研究结果表明,circ_0007765通过吸附miR-654-3p提高了FRS2的表达,从而促进了PDGF-BB诱导的HA-VSMC的增殖和迁移,为强直性脊柱炎提供了一种可行的治疗策略。
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引用次数: 0
Potential Role of Dipeptidyl Peptidase-4 in Regulating Mitochondria and Oxidative Stress in Cardiomyocytes. 二肽基肽酶-4 在调节线粒体和心肌细胞氧化应激中的潜在作用
IF 3.4 3区 医学 Q2 CARDIAC & CARDIOVASCULAR SYSTEMS Pub Date : 2024-10-01 Epub Date: 2024-07-02 DOI: 10.1007/s12012-024-09884-z
Shih-Yi Lee, Shao-Tung Wu, Chen-Xuan Du, Hui-Chun Ku

Oxidative stress causes mitochondrial damage and bioenergetic dysfunction and inhibits adenosine triphosphate production, contributing to the pathogenesis of cardiac diseases. Dipeptidyl peptidase 4 (DPP4) is primarily a membrane-bound extracellular peptidase that cleaves Xaa-Pro or Xaa-Ala dipeptides from the N terminus of polypeptides. DPP4 inhibitors have been used in patients with diabetes and heart failure; however, they have led to inconsistent results. Although the enzymatic properties of DPP4 have been well studied, the substrate-independent functions of DPP4 have not. In the present study, we knocked down DPP4 in cultured cardiomyocytes to exclude the effects of differential alteration in the substrates and metabolites of DPP4 then compared the response between the knocked-down and wild-type cardiomyocytes during exposure to oxidative stress. H2O2 exposure induced DPP4 expression in both types of cardiomyocytes. However, knocking down DPP4 substantially reduced the loss of cell viability by preserving mitochondrial bioenergy, reducing intracellular reactive oxygen species production, and reducing apoptosis-associated protein expression. These findings demonstrate that inhibiting DPP4 improves the body's defense against oxidative stress by enhancing Nrf2 and PGC-1α signaling and increasing superoxide dismutase and catalase activity. Our results indicate that DPP4 mediates the body's response to oxidative stress in individuals with heart disease.

氧化应激会造成线粒体损伤和生物能功能障碍,并抑制三磷酸腺苷的产生,从而导致心脏疾病的发病机理。二肽基肽酶 4(DPP4)主要是一种膜结合细胞外肽酶,可从多肽的 N 端裂解 Xaa-Pro 或 Xaa-Ala 二肽。DPP4 抑制剂已用于糖尿病和心力衰竭患者,但效果并不一致。尽管对 DPP4 的酶学特性进行了深入研究,但对 DPP4 与底物无关的功能却没有深入研究。在本研究中,我们敲除了培养的心肌细胞中的 DPP4,以排除 DPP4 底物和代谢产物的不同改变的影响,然后比较了被敲除的心肌细胞和野生型心肌细胞在暴露于氧化应激时的反应。H2O2暴露诱导了两种类型心肌细胞中DPP4的表达。然而,通过保护线粒体生物能、减少细胞内活性氧的产生和降低细胞凋亡相关蛋白的表达,敲除 DPP4 大大降低了细胞活力的丧失。这些研究结果表明,抑制 DPP4 可增强 Nrf2 和 PGC-1α 信号转导,提高超氧化物歧化酶和过氧化氢酶的活性,从而改善机体对氧化应激的防御能力。我们的研究结果表明,DPP4 在心脏病患者体内介导机体对氧化应激的反应。
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引用次数: 0
Association Between CYP2D7 and TCF20 Polymorphisms and Coronary Heart Disease. CYP2D7 和 TCF20 多态性与冠心病的关系
IF 3.4 3区 医学 Q2 CARDIAC & CARDIOVASCULAR SYSTEMS Pub Date : 2024-10-01 Epub Date: 2024-07-26 DOI: 10.1007/s12012-024-09907-9
Wenjie Zhang, Panpan Wan, Man Zhang, Yanting Chang, Shuli Du, Tianbo Jin, Yuan Wang

One of the causes of coronary heart disease (CHD) is genetic factors. In this study, we explored the relationship between CYP2D7 and TCF20 gene polymorphisms and the risk of CHD in the Han Chinese population. Three single nucleotide polymorphisms (CYP2D7 rs1800754, CYP2D7 rs2743461, and TCF20 rs760648) were selected and genotyped from 490 cases and 480 controls. The odds ratios (ORs) and 95% confidence intervals (CIs) were used to assess the association between CYP2D7 and TCF20 polymorphisms and the risk of CHD. The association between clinical indicators and polymorphisms was analyzed using one-way ANOVA and Tukey's HSD. The SNP-SNP interactions were obtained by performing multifactor dimensionality reduction (MDR). CYP2D7 rs1800754 and rs2743461 were closely associated with increased risk of CHD (alleles: p = 0.014, p = 0.031). Stratified analysis showed that CYP2D7 rs1800754 and rs2743461 were associated with an increased risk of CHD in men, age > 60 years, BMI ≥ 24, and smoking. Rs1800754 is also associated with an increased risk of CHD associated with alcohol consumption. In addition, TCF20 rs760648 was associated with a reduced risk of CHD in patients aged ≤ 60 years and with CALs. A significant association was found between CYP2D7 rs1800754 and rs2743461 genotypes and levels of UREA, Cr, and LDL-C; TCF20 rs760648 genotypes and levels of RBC. The MDR analysis showed that the three-locus interaction model was the best in the multi-locus model. In conclusion, CYP2D7 rs1800754 and rs2743461 polymorphisms were associated with CHD risk.

冠心病(CHD)的病因之一是遗传因素。本研究探讨了中国汉族人群中 CYP2D7 和 TCF20 基因多态性与冠心病风险之间的关系。研究选取了 490 例病例和 480 例对照中的三个单核苷酸多态性(CYP2D7 rs1800754、CYP2D7 rs2743461 和 TCF20 rs760648)进行基因分型。采用几率比(ORs)和 95% 置信区间(CIs)来评估 CYP2D7 和 TCF20 多态性与冠心病风险之间的关系。临床指标与多态性之间的关联采用单因素方差分析和Tukey's HSD进行分析。通过多因素降维(MDR)获得了SNP-SNP相互作用。CYP2D7 rs1800754 和 rs2743461 与冠心病风险增加密切相关(等位基因:p = 0.014,p = 0.031)。分层分析表明,CYP2D7 rs1800754 和 rs2743461 与男性、年龄大于 60 岁、体重指数≥ 24 和吸烟者的冠心病风险增加有关。Rs1800754 还与饮酒导致的冠心病风险增加有关。此外,TCF20 rs760648 与年龄≤60 岁和有 CALs 的患者的冠心病风险降低有关。研究发现,CYP2D7 rs1800754和rs2743461基因型与UREA、Cr和LDL-C水平;TCF20 rs760648基因型与RBC水平之间存在明显关联。MDR 分析表明,三病灶交互作用模型在多病灶模型中是最好的。总之,CYP2D7 rs1800754和rs2743461多态性与冠心病风险相关。
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引用次数: 0
Association Between the Copper-to-Zinc Ratio and Cardiovascular Disease Among Chinese Adults: A China Multi-ethnic Cohort (CMEC) Study. 中国成年人铜锌比值与心血管疾病之间的关系:中国多民族队列(CMEC)研究》。
IF 3.4 3区 医学 Q2 CARDIAC & CARDIOVASCULAR SYSTEMS Pub Date : 2024-10-01 Epub Date: 2024-08-12 DOI: 10.1007/s12012-024-09904-y
Yili Shen, Yuxin Hu, Leilei Liu, Jianqin Zhong, Yuxin Zhang, Shenyan Wu, Cheng Chen, Feng Hong

The impact of metal exposure on cardiovascular diseases has become an increasingly concerning topic. To date, few studies have investigated the relationship between the copper-to-zinc ratio and CVD (Cardiovascular disease). This China multi-ethnic cohort study explored the association between the copper-to-zinc ratio and CVD in Chinese adults. The study included a sample size of 9878 people. Logistic regression analysis was used to examine the correlation between urinary copper, urinary zinc, and the copper-to-zinc ratio and CVD prevalence. Restricted cubic spline (RCS) analysis was used to investigate the potential dose-response relationships among copper-to-zinc ratio, urinary copper, urinary zinc, and CVD prevalence. In addition, the least absolute shrinkage and selection operator (LASSO) regression method was used to identify significant risk factors associated with CVD, leading to the development of a nomogram. The predictive performance of the nomogram model for CVD was assessed using the receiver operating characteristic (ROC) curve and the area under the curve (AUC). Compared with the copper-to-zinc ratio in Q1, the copper-to-zinc ratio in Q4 was associated with CVD after adjusting for all potential confounders (Model 3) (Q4, odds ratio [OR] 0.608, 95% confidence interval [CI] 0.416-0.889, P = 0.010). After adjusting for all potential confounders (Model 3), urinary copper levels in Q4 were associated with CVD (Q4, odds ratio [OR] 0.627, 95% confidence interval [CI] 0.436-0.902, P = 0.012). No significant difference was found between urinary zinc levels and CVD. The RCS showed a linear dose-response relationship between the copper-to-zinc ratio and CVD (P for overall = 0.01). The nomogram based on the influencing factors examined with LASSO showed good predictive power, and the AUC was 76.3% (95% CI 73.7-78.9%). Our results suggest that there is a significant linear negative correlation between the copper-to-zinc ratio and CVD in Chinese adults and that it has good predictive value for CVD.

金属暴露对心血管疾病的影响已成为一个越来越受关注的话题。迄今为止,很少有研究调查铜锌比值与心血管疾病(CVD)之间的关系。这项中国多民族队列研究探讨了铜锌比值与中国成年人心血管疾病之间的关系。该研究的样本量为 9878 人。研究采用逻辑回归分析法来检验尿铜、尿锌、铜锌比值与心血管疾病患病率之间的相关性。限制立方样条(RCS)分析用于研究铜锌比值、尿铜、尿锌和心血管疾病患病率之间的潜在剂量反应关系。此外,还采用了最小绝对收缩和选择算子(LASSO)回归法来确定与心血管疾病相关的重要风险因素,从而建立了一个提名图。利用接收者操作特征曲线(ROC)和曲线下面积(AUC)评估了提名图模型对心血管疾病的预测性能。与第一季度的铜锌比值相比,第四季度的铜锌比值在调整所有潜在混杂因素(模型 3)后与心血管疾病相关(第四季度,几率比 [OR] 0.608,95% 置信区间 [CI] 0.416-0.889,P = 0.010)。调整所有潜在混杂因素(模型 3)后,第四季度的尿铜水平与心血管疾病相关(第四季度,几率比 [OR] 0.627,95% 置信区间 [CI] 0.436-0.902,P = 0.012)。尿锌水平与心血管疾病之间无明显差异。RCS显示铜锌比值与心血管疾病之间存在线性剂量反应关系(总体P = 0.01)。基于 LASSO 检测的影响因素的提名图显示出良好的预测能力,AUC 为 76.3% (95% CI 73.7-78.9%)。我们的研究结果表明,铜锌比值与中国成年人心血管疾病之间存在显著的线性负相关,对心血管疾病具有良好的预测价值。
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Cardiovascular Toxicology
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