Journal of molecular and cellular cardiology plus最新文献

英文中文

Disruption of ventricular activation by subthreshold delayed afterdepolarizations in RyR2-R420Q catecholaminergic polymorphic ventricular tachycardia RyR2-R420Q儿茶酚胺能多形性室性心动过速的阈下延迟后去极化对心室激活的破坏

Journal of molecular and cellular cardiology plus

Pub Date : 2025-06-11 DOI: 10.1016/j.jmccpl.2025.100466

Ewan D. Fowler , Salimata L. Diakite , Ana M. Gomez , Michael A. Colman

Background

Catecholaminergic polymorphic ventricular tachycardia (CPVT) carries increased risk of ventricular arrhythmias due to altered Ca²⁺ regulation associated with mutations in the ryanodine receptor (RyR2). Increased Ca²⁺ leak is believed to result in diastolic Ca²⁺ waves and delayed afterdepolarization (DADs) in cardiac myocytes, but it is uncertain how these cellular events induce ventricular tachycardia in the whole heart. We utilised a transgenic mouse model of human RyR2-R420Q (R420Q) CPVT mutation and a range of electrical and optical mapping technologies to examine the role of DAD-induced conduction abnormalities.

Methods

Heterozygous R420Q and wildtype (WT) control hearts were perfused on a Langendorff apparatus. Electrical activity was monitored using volume conducted ECG electrodes and monophasic action potential (MAP) electrode recordings. Left ventricular activation and membrane potential changes were recorded using an 8 × 8 multielectrode array and optical mapping, respectively.

Results

ECG recordings showed spontaneous ventricular arrhythmias in isolated R420Q hearts. More severe arrhythmias occurred in R420Q hearts following rapid electrical pacing combined with isoproterenol stimulation. Ventricular activation time was not different between genotypes, regardless of stimulation frequency or isoproterenol. Phase differences in local activation times were greater in R420Q hearts during 10 Hz pacing with isoproterenol, suggesting local conduction slowing. Optical mapping experiments revealed subthreshold DADs occurring in R420Q hearts during diastolic pauses. DADs prolonged the subsequent action potential and were associated with conduction slowing during the second beat after the DAD, but not the first beat. 2D tissue simulations revealed that direct inactivation of I_Na during DADs, or indirectly via cycle length dependent refractory mechanisms could account for local conduction slowing.

Conclusions

Increased activation dispersion could arise from subthreshold DADs in R420Q mouse hearts and may contribute to conduction block. This could increase the propensity for re-entrant arrhythmias in CPVT without directly triggering ectopic beats.

儿茶酚胺能多态性室性心动过速（CPVT）由于与ryanodine受体（RyR2）突变相关的Ca2+调节改变而增加室性心律失常的风险。增加的Ca2+泄漏被认为会导致心肌细胞舒张期Ca2+波和延迟后去极化（DADs），但不确定这些细胞事件如何诱导整个心脏的室性心动过速。我们利用人类RyR2-R420Q (R420Q) CPVT突变转基因小鼠模型和一系列电学和光学定位技术来研究dad诱导的传导异常的作用。方法在Langendorff仪上灌注异合子R420Q和野生型（WT）对照心脏。电活动监测采用体积传导ECG电极和单相动作电位（MAP）电极记录。采用8 × 8多电极阵列和光学成像分别记录左心室激活和膜电位变化。结果在离体R420Q心脏中出现自发性室性心律失常。快速电起搏联合异丙肾上腺素刺激后，R420Q心脏发生更严重的心律失常。与刺激频率或异丙肾上腺素无关，不同基因型的心室激活时间无差异。在10hz异丙肾上腺素起搏时，R420Q心脏局部激活时间的相位差更大，表明局部传导减慢。光学测绘实验显示，R420Q心脏在舒张期暂停时发生阈下DADs。DADs延长了随后的动作电位，并与DAD后第二次心跳的传导减慢有关，但与第一次心跳无关。二维组织模拟显示，在DADs期间，INa的直接失活，或间接通过周期长度依赖的难熔机制，可以解释局部传导减慢。结论R420Q小鼠心脏阈下DADs激活弥散度增加，可能导致传导阻滞。这可能会增加CPVT再入性心律失常的倾向，而不会直接引发异位搏。

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引用次数: 0

Blueprint of the distinct metabolite profiles of healthy pig heart chambers 健康猪心腔不同代谢物谱的蓝图

Journal of molecular and cellular cardiology plus

Pub Date : 2025-06-10 DOI: 10.1016/j.jmccpl.2025.100462

Retu Haikonen , Topi Meuronen , Ville Koistinen , Olli Kärkkäinen , Tomi Tuomainen , Gloria I Solano-Aguilar , Joseph F. Urban Jr. , Marko Lehtonen , Pasi Tavi , Kati Hanhineva

The heart is one of the most studied organs, with physiological processes and disease research. While it is well-established that significant structural and functional differences exist between the chambers, most studies focus on only a single heart chamber, predominantly the left ventricle. This study aims to comprehensively characterise the chamber-specific metabolic profiles of all four heart chambers in a healthy animal model close to human metabolism, pigs. We employed liquid chromatography-mass spectrometry metabolomics to analyse the metabolite profiles of heart chambers in healthy pigs (N = 30) maintained on an ad libitum diet and housed under standard, non-stressed physiological conditions. Our findings reveal a higher energy demand in the left ventricle, as evidenced by elevated levels of electron transport chain-related metabolites such as NAD⁺ and FAD. Additionally, hexose-phosphates and several acylcarnitines exhibited chamber-dependent variations in abundance. The ventricles, particularly the left, demonstrated distinct redox states, with differential levels of glutathione and ascorbic acid, suggesting variations in oxidative stress across chambers. Furthermore, amino acids had chamber-specific abundance patterns, and ventricles showed an increased requirement for protein synthesis, likely associated with repair mechanisms following reactive oxygen species (ROS)-induced cellular damage. Our study reveals significant differences in the metabolic profiles across four heart chambers in healthy pig hearts, underscoring the metabolic heterogeneity of cardiac tissue. These findings highlight the necessity of investigating chamber-specific metabolic pathways to better understand heart functionality. Such insights could inform the development of more precise therapeutic strategies tailored to metabolic demands and functional roles in heart chambers.

心脏是研究最多的器官之一，有生理过程和疾病研究。虽然心室之间存在显著的结构和功能差异是公认的，但大多数研究只关注单个心脏腔，主要是左心室。本研究旨在全面表征所有四个心脏腔室的代谢特征，在接近人类代谢的健康动物模型中，猪。我们采用液相色谱-质谱代谢组学分析了30头健康猪（N = 30）的心脏室代谢物谱，这些猪饲喂自由饮食，饲养在标准的非应激生理条件下。我们的研究结果揭示了左心室更高的能量需求，正如电子传递链相关代谢物如NAD+和FAD水平升高所证明的那样。此外，己糖磷酸和几种酰基肉碱的丰度表现出室依赖性变化。心室，尤其是左心室，表现出不同的氧化还原状态，谷胱甘肽和抗坏血酸水平不同，表明不同心室的氧化应激存在差异。此外，氨基酸具有室特异性丰度模式，心室对蛋白质合成的需求增加，这可能与活性氧（ROS）诱导的细胞损伤后的修复机制有关。我们的研究揭示了健康猪心脏中四个心脏腔的代谢谱存在显著差异，强调了心脏组织的代谢异质性。这些发现强调了研究室特异性代谢途径以更好地了解心脏功能的必要性。这些见解可以为更精确的治疗策略的发展提供信息，这些治疗策略可以根据心脏腔内的代谢需求和功能角色量身定制。

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引用次数: 0

Ultrastructure analysis of mitochondria, lipid droplet and sarcoplasmic reticulum apposition in human heart failure 人心力衰竭时线粒体、脂滴及肌浆网附着的超微结构分析

Journal of molecular and cellular cardiology plus

Pub Date : 2025-06-10 DOI: 10.1016/j.jmccpl.2025.100461

Nadina R. Latchman , Tyler L. Stevens , Kenneth C. Bedi , Benjamin L. Prosser , Kenneth B. Margulies , John W. Elrod

Background

Cardiomyocyte structural remodeling is reported as a causal contributor to heart failure (HF) development and progression. Growing evidence highlights the role of organelle apposition in cardiomyocyte function and homeostasis. Disruptions in organelle crosstalk, such as that between the sarcoplasmic reticulum (SR) and mitochondria, dysregulate numerous cellular processes that include calcium handling and cellular bioenergetics, two processes that are disrupted and implicated in cardiac pathophysiology. While the physical distance between organelles is thought to be essential for homeostatic cardiomyocyte function, whether the interactions and coupling of organelles are altered in human heart failure remains unclear.

Methods

Here, we utilized transmission electron microscopy to characterize the role of organelle apposition in cardiomyocytes from patients with various etiologies of HF. Subsequently, we employed molecular approaches to examine expression changes of proposed organelle tethers.

Results

We demonstrate that cardiomyocytes from dilated cardiomyopathy, hypertrophic cardiomyopathy and ischemic cardiomyopathy hearts display smaller, rounded mitochondria as compared to nonfailing controls. Failing cardiomyocytes also exhibited disrupted SR-mitochondria juxtaposition and changes in the expression of various proposed molecular tethers. Further analysis revealed alterations in lipid droplet dynamics including decreased lipid droplet number and less lipid droplets in association with mitochondria in failing cardiomyocytes.

Conclusion

We observed dysregulated organelle dynamics which was conserved across various etiologies of heart failure. Our results suggest that organelle structure and apposition is a possible contributor to human HF progression.

背景心肌细胞结构重塑被认为是心力衰竭（HF）发生和发展的一个原因。越来越多的证据强调了细胞器在心肌细胞功能和稳态中的作用。细胞器串扰的破坏，如肌浆网（SR）和线粒体之间的串扰，会导致许多细胞过程失调，包括钙处理和细胞生物能量学，这两个过程被破坏并与心脏病理生理有关。虽然细胞器之间的物理距离被认为对稳态心肌细胞功能至关重要，但在人类心力衰竭中，细胞器的相互作用和偶联是否发生了改变尚不清楚。方法在此，我们利用透射电子显微镜来表征各种病因的心衰患者心肌细胞中细胞器附着的作用。随后，我们采用分子方法检测细胞器系链的表达变化。结果我们证明，扩张型心肌病、肥厚型心肌病和缺血性心肌病心脏的心肌细胞与非衰竭对照组相比，线粒体更小、更圆。衰竭的心肌细胞也表现出中断的sr -线粒体并置和各种分子链表达的变化。进一步的分析揭示了脂滴动力学的改变，包括脂滴数量的减少和与衰竭心肌细胞线粒体相关的脂滴减少。结论我们观察到细胞器动力学异常在各种心力衰竭病因中都是保守的。我们的研究结果表明，细胞器结构和对立可能是人类HF进展的一个因素。

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引用次数: 0

Genetic deletion or pharmacological inhibition of acetyl-CoA carboxylase 2 enhances fatty acid oxidation and improves cardiac function and survival in the murine ATGL knockout model of severe heart failure 在严重心力衰竭小鼠ATGL敲除模型中，乙酰辅酶a羧化酶2基因缺失或药理抑制可增强脂肪酸氧化，改善心功能和生存率

Journal of molecular and cellular cardiology plus

Pub Date : 2025-06-02 DOI: 10.1016/j.jmccpl.2025.100459

Mai Usui , Yu Tsurekawa , Tatsuya Ikehara , Atsuyuki Shimazaki , Archana Vijayakumar , Robert P. Myers , G. Mani Subramanian , Eisuke Murakami

Impaired myocardial energetics, including fatty acid oxidation (FAO), is a hallmark feature in the pathophysiology of various disorders. Deficiency of adipose triglyceride lipase (ATGL) results in impaired FAO which leads to severe heart failure due to massive triglyceride accumulation in cardiac muscle and coronary vasculature. Acetyl-CoA carboxylase 2 (ACC2) is a mitochondrial enzyme that regulates FAO; ACC2 inhibition increases transport of fatty acids into mitochondria for oxidation. In this study, the murine ATGL knockout (KO) model of severe heart failure was used to evaluate the effects ACC2 inhibition induced by whole body genetic KO (Atgl/Acc2 double KO mice) and pharmacological inhibition with TLC-3595, an oral, selective small molecule inhibitor of ACC2. Both genetic deletion of Acc2 and treatment with TLC-3595 in Atgl KO mice promoted mitochondrial FAO, reduced cardiac lipid accumulation and remodeling, and led to significant improvements in cardiac function, locomotor activity, and survival. Metabolite profiling of cardiac tissue of Atgl/Acc2 double KO mice and Atgl KO mice treated with TLC-3595 revealed ACC2-specific changes, including reduced malonyl-CoA and increased short-, medium-, and long-chain acylcarnitines, consistent with improved FAO. These findings support the therapeutic targeting of ACC2 for the treatment of heart failure associated with impaired FAO.

心肌能量受损，包括脂肪酸氧化（FAO），是各种疾病病理生理学的一个标志性特征。脂肪甘油三酯脂肪酶（ATGL）缺乏会导致FAO受损，从而由于心肌和冠状血管中大量甘油三酯积累而导致严重的心力衰竭。乙酰辅酶a羧化酶2 （ACC2）是一种线粒体酶，可调节FAO；ACC2抑制增加脂肪酸进入线粒体氧化的运输。本研究采用小鼠重度心力衰竭ATGL敲除（KO）模型，评价全身遗传性KO （ATGL / ACC2双KO小鼠）对ACC2的抑制作用以及口服选择性ACC2小分子抑制剂TLC-3595的药理抑制作用。在Atgl KO小鼠中，Acc2基因缺失和TLC-3595处理均可促进线粒体FAO，减少心脏脂质积累和重塑，并显著改善心功能、运动活性和生存率。Atgl/Acc2双KO小鼠和TLC-3595处理的Atgl KO小鼠心脏组织代谢物谱显示Acc2特异性变化，包括丙二酰辅酶a减少，短链、中链和长链酰基肉碱增加，与改善的FAO一致。这些发现支持将ACC2靶向治疗与粮农组织受损相关的心力衰竭。

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引用次数: 0

Is boosting OXPHOS/FAO gene pathways the final end-mechanism of SGLT2i protection? 促进OXPHOS/FAO基因通路是SGLT2i保护的最终机制吗？

Journal of molecular and cellular cardiology plus

Pub Date : 2025-06-01 DOI: 10.1016/j.jmccpl.2025.100297

Xin Hu, Coert J. Zuurbier

引用次数: 0

Elucidating the transcriptional and epigenetic impact of succinate dehydrogenase inhibition on cardiac regeneration 阐明琥珀酸脱氢酶抑制对心脏再生的转录和表观遗传学影响

Journal of molecular and cellular cardiology plus

Pub Date : 2025-06-01 DOI: 10.1016/j.jmccpl.2025.100344

Dakota Nuttall, Ahmed Mahmoud

引用次数: 0

Another-regulin regulates cardiomyocyte calcium handling via integration of neuroendocrine signaling with SERCA2a activity 另一种调节蛋白通过神经内分泌信号与SERCA2a活性的整合来调节心肌细胞钙处理

Journal of molecular and cellular cardiology plus

Pub Date : 2025-06-01 DOI: 10.1016/j.jmccpl.2025.100386

Keira Hassel , Aaron Gibson , Jaroslava Seflova , Ellen Cho , N. Scott Blair , Douglas Anderson , Seth Robia , Catherine Makarewich

引用次数: 0

Mechanical Load Induces Insulin Resistance in Adult Cardiomyocytes via Cell Autonomous and Microtubule-Dependent Mechanisms 机械负荷通过细胞自主和微管依赖机制诱导成人心肌细胞胰岛素抵抗

Journal of molecular and cellular cardiology plus

Pub Date : 2025-06-01 DOI: 10.1016/j.jmccpl.2025.100380

Alexia Vite, Nesrine Bouhrira, Deborah Eaton, Kenneth Bedi, Keita Uchida, Benjamin Prosser, Zoltan Arany, Kenneth Marguliea

引用次数: 0

Post-transcriptional regulation of gene expression by ribosome-binding protein 1 核糖体结合蛋白对基因表达的转录后调控

Journal of molecular and cellular cardiology plus

Pub Date : 2025-06-01 DOI: 10.1016/j.jmccpl.2025.100361

Marjan Aghajani , Eric Schoger , Federico Bleckwedel , Julia Groß , Nicole Herzog , Mirko Völkers , Tobias Jakobi , Laura Zelarayan , Shirin Doroudgar

引用次数: 0

Derivation of a Comprehensive Biobank of Human iPSC Lines for Open-Access Distribution to Academic Researchers 为学术研究人员开放获取分发的人类iPSC系的综合生物库的推导

Journal of molecular and cellular cardiology plus

Pub Date : 2025-06-01 DOI: 10.1016/j.jmccpl.2025.100408

Christopher Yan , Celine Lai , Sushma Shenoy , Rebecca Yu , Zachary Cook , Julio Guevara , Yan Zhuge , Joseph Wu , Paul Pang

引用次数: 0

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全部化学•材料生命科学医学物理工程技术环境•农林材料科学地球科学法学管理学化学环境科学与生态学计算机科学教育学经济学农林科学人文科学生物学数学物理与天体物理心理学综合性期刊其他工业工程理学历史学农学文学信息工程

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Journal of molecular and cellular cardiology plus

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