Journal of molecular and cellular cardiology plus最新文献

英文中文

Circulating autophagy regulator Rubicon is linked to increased myocardial infarction risk 循环中的自噬调节因子 Rubicon 与心肌梗死风险增加有关。

Journal of molecular and cellular cardiology plus

Pub Date : 2024-12-21 DOI: 10.1016/j.jmccpl.2024.100279

Marie-Hélène Grazide , Jean-Bernard Ruidavets , Wim Martinet , Meyer Elbaz , Cécile Vindis

Background

The identification of new biomarkers that improve existing cardiovascular risk prediction models for acute coronary syndrome is essential for accurately identifying high-risk patients and refining treatment strategies. Autophagy, a vital cellular degradation mechanism, is important for maintaining cardiac health. Dysregulation of autophagy has been described in cardiovascular conditions such as myocardial ischemia-reperfusion injury, a key factor in myocardial infarction (MI). Recently, Rubicon (Run domain Beclin-1-interacting and cysteine-rich domain-containing protein), a key negative regulator of autophagy, has been identified in the modulation of cardiac stress response.

Objectives

This study aimed to explore the relationship between circulating Rubicon levels and MI, and to evaluate the incremental predictive value of Rubicon when integrated into a clinical risk prediction model for MI.

Results

We analyzed plasma Rubicon concentrations in 177 participants, comprising type I MI patients and high-risk control subjects. Our results revealed significantly elevated plasma Rubicon levels in MI patients compared to the control group (126.5 pg/mL vs. 53 pg/mL, p < 0.001). Furthermore, Rubicon levels showed a positive correlation with cardiovascular risk factors such as total cholesterol and LDL cholesterol. Multivariate analysis confirmed that Rubicon levels were independently associated with an increased risk of MI. The inclusion of Rubicon in traditional cardiovascular risk models notably enhanced predictive accuracy for MI, with the area under the curve (AUC) rising from 0.868 to 0.905 (p < 0.001).

Conclusions

These findings suggest that Rubicon is a valuable biomarker associated with MI risk, providing additional predictive value beyond standard cardiovascular risk factors. This highlights the importance of Rubicon's critical role in the pathophysiology of CVD.

背景：确定新的生物标志物以改进现有的急性冠状动脉综合征心血管风险预测模型，对于准确识别高危患者和改进治疗策略至关重要。自噬是一种重要的细胞降解机制，对维持心脏健康非常重要。自噬失调已在心血管疾病中得到描述，如心肌缺血再灌注损伤，这是心肌梗塞（MI）的一个关键因素。最近，Rubicon（Run domain Beclin-1-interacting and cysteine-rich domain-containing protein）作为自噬的一个关键负调控因子被发现参与了心脏应激反应的调节：本研究旨在探讨循环Rubicon水平与心肌梗死之间的关系，并评估Rubicon纳入心肌梗死临床风险预测模型后的增量预测价值：我们分析了177名参与者的血浆Rubicon浓度，其中包括I型心肌梗死患者和高风险对照受试者。结果显示，与对照组相比，心肌梗死患者的血浆 Rubicon 水平明显升高（126.5 pg/mL vs. 53 pg/mL，p p 结论：这些发现表明，Rubicon 是心肌梗死临床风险预测模型的一个重要组成部分：这些研究结果表明，Rubicon 是一种与心肌梗死风险相关的有价值的生物标志物，在标准心血管风险因素之外还具有额外的预测价值。这凸显了 Rubicon 在心血管疾病病理生理学中的重要作用。

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引用次数: 0

Cardioprotective strategies in myocardial ischemia-reperfusion injury: Implications for improving clinical translation

Journal of molecular and cellular cardiology plus

Pub Date : 2024-12-16 DOI: 10.1016/j.jmccpl.2024.100278

Chao Tong , Bingying Zhou

Ischemic heart disease is the most common cause of death and disability globally which is caused by reduced or complete cessation of blood flow to a portion of the myocardium. One of its clinical manifestations is myocardial infarction, which is commonly treated by restoring of blood flow through reperfusion therapies. However, serious ischemia-reperfusion injury (IRI) can occur, significantly undermining clinical outcomes, for which there is currently no effective therapy. This review revisits several potential pharmacological IRI intervention strategies that have entered preclinical or clinical research phases. Here, we discuss what we have learned through translational failures over the years, and propose possible ways to enhance translation efficiency.

引用次数: 0

An optimized plasmalogen modulating dietary supplement provides greater protection in a male than female mouse model of dilated cardiomyopathy 一种优化的调节性膳食补充剂对扩张型心肌病的雄性小鼠模型提供了比雌性小鼠更大的保护。

Journal of molecular and cellular cardiology plus

Pub Date : 2024-12-04 DOI: 10.1016/j.jmccpl.2024.100273

Teleah G. Belkin , Emma I. Masterman , Gunes S. Yildiz , Helen Kiriazis , Natalie A. Mellett , Jonathon Cross , Kyah Grigolon , Akshima Dogra , Daniel Donner , Roger Chooi , Amy Liang , Andrew R. Kompa , Junichi Sadoshima , Amanda J. Edgley , David W. Greening , Peter J. Meikle , Yow Keat Tham , Julie R. McMullen

We previously reported that plasmalogens, a class of phospholipids, were decreased in a setting of dilated cardiomyopathy (DCM). Plasmalogen levels can be modulated via a dietary supplement called alkylglycerols (AG) which has demonstrated benefits in some disease settings. However, its therapeutic potential in DCM remained unknown. To determine whether an optimized AG supplement could restore plasmalogen levels and attenuate cardiac dysfunction/pathology, we placed a cardiac-specific transgenic DCM mouse model of both sexes on chow +/−1.5 % AG supplementation at ∼10 weeks of age for 16 weeks. Cardiac function was assessed by echocardiography, tissues were collected for histological and molecular analyses including lipidomics and proteomics via liquid chromatography-mass spectrometry. AG supplementation increased total plasmalogens in DCM hearts and attenuated lung congestion of both sexes, but only prevented cardiac dysfunction in males. This was associated with attenuated cardiac and renal enlargement, a more favorable pro-cardiac gene expression profile, and a trend for lower cardiac fibrosis. By lipidomics, specific d18:1 ceramide species associated with cardiac pathology were lower in the DCM hearts from mice on the AG diet, and tetralinoleoyl cardiolipins, a lipid crucial for mitochondrial function was restored with AG supplementation. Proteomic analysis of hearts from male DCM mice receiving AG supplementation revealed enrichment in mitochondrial protein network, as well as upregulation of extracellular matrix binding proteins including agrin, a protein associated with cardiac regeneration. In summary, AG supplementation restored plasmalogens in DCM hearts but showed greater therapeutic potential in males than females.

我们以前曾报道过，在扩张型心肌病（DCM）的病例中，磷脂类物质质粒减少。质粒蛋白的水平可以通过一种名为烷基甘油（AG）的膳食补充剂来调节，这种补充剂在某些疾病的治疗中已被证明是有益的。然而，它在 DCM 中的治疗潜力仍然未知。为了确定优化的 AG 补充剂是否能恢复质原水平并减轻心脏功能障碍/病理变化，我们让一只心脏特异性转基因 DCM 小鼠（雌雄均可）在 10 周大时服用饲料 +/-1.5% AG 补充剂，连续服用 16 周。通过超声心动图评估心脏功能，收集组织进行组织学和分子分析，包括通过液相色谱-质谱进行脂质组学和蛋白质组学分析。补充 AG 可增加 DCM 心脏的总浆醛酸，减轻男女肺充血，但只能预防男性的心功能障碍。这与减轻心脏和肾脏肿大、更有利的促心脏基因表达谱以及降低心脏纤维化的趋势有关。通过脂质组学分析，与心脏病理学相关的特定 d18:1 神经酰胺种类在摄入 AG 饮食的 DCM 小鼠心脏中含量较低，而对线粒体功能至关重要的脂质--四亚油酰心磷脂在补充 AG 后得到恢复。对补充 AG 的雄性 DCM 小鼠心脏进行的蛋白质组分析表明，线粒体蛋白网络丰富，细胞外基质结合蛋白（包括与心脏再生相关的蛋白 agrin）上调。总之，补充 AG 可恢复 DCM 心脏的质粒，但对雄性小鼠的治疗潜力大于雌性小鼠。

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引用次数: 0

10038: Myosin Inhibition using mavacamten facilitates relaxation and improves compliance of the myofibrils from the HFpEF heart

Journal of molecular and cellular cardiology plus

Pub Date : 2024-12-01 DOI: 10.1016/j.jmccpl.2024.100160

YH Lin, EP Yap, S Cong, G Sivakumar, NGZ Tee, CJA Ramachandra, DJ Hausenloy

引用次数: 0

10055: Cardiac Disease Occurrences in Primary Aldosteronism patients at Hospital Canselor Tuanku Muhriz UKM: Comparison of Unilateral versus Bilateral Subtype and Medical Treatment versus Adrenalectomy

Journal of molecular and cellular cardiology plus

Pub Date : 2024-12-01 DOI: 10.1016/j.jmccpl.2024.100177

Aina Nadheera Abd Rahman, Megan Limbang, Haritha Subba Rau, Hazim Fadzli, Yue Zhen Lim, Adi Syazni Muhammed, Norlela Sukor, Elena Aisha Azizan

引用次数: 0

10049: Human PSC-based engineered heart tissue platform for disease modeling and investigation of new gene candidates in heart diseases

Journal of molecular and cellular cardiology plus

Pub Date : 2024-12-01 DOI: 10.1016/j.jmccpl.2024.100171

Rujie Qi, Roger Foo, Matthew Ackers-Johnson

引用次数: 0

10020: Identification of a novel enhancer to drive robust cardiac specific gene expression

Journal of molecular and cellular cardiology plus

Pub Date : 2024-12-01 DOI: 10.1016/j.jmccpl.2024.100142

Michelle C.E. Mak, Roger S.Y. Foo

引用次数: 0

10007: Targeting EIF5A hypusination to improve protein synthesis and mitochondrial function during MASH

Journal of molecular and cellular cardiology plus

Pub Date : 2024-12-01 DOI: 10.1016/j.jmccpl.2024.100129

Jeremy Pang, Madhulika Tripathi, Jia Pei Ho, Anissa Widjaja, Shamini Guna Shekeran, Stuart Alexander Cook, Ayako Suzuki, Anna Mae Diehl, Enrico Petretto, Brijesh Kumar Singh, Paul Michael Yen, Jin Zhou

引用次数: 0

Increased perivascular fibrosis and pro-fibrotic cellular transition in intramyocardial blood vessels in myocardial infarction patients 心肌梗死患者心内血管血管周围纤维化和前纤维化细胞转变增加。

Journal of molecular and cellular cardiology plus

Pub Date : 2024-12-01 DOI: 10.1016/j.jmccpl.2024.100275

Zhu Jiang , Giulia Sorrentino , Suat Simsek , Joris J.T.H. Roelofs , Hans W.M. Niessen , Paul A.J. Krijnen

Background and objectives

Structural and functional changes in the intramyocardial microcirculation increase the risk of myocardial infarction (MI). This study investigated intramyocardial perivascular fibrosis and pro-fibrotic cellular transitions in deceased acute and subacute MI patients to explore their involvement in the pathogenesis of MI.

Methods

Left ventricular tissue (LV) was obtained from the infarction area of autopsied patients with acute-phase MI (3–6 h; n = 24), subacute-phase MI (5–14 days; n = 12), and noninfarcted controls (n = 14). Perivascular fibrosis and fibroblast activation protein (FAP) expression were quantified using (immuno)histochemistry. Fibroblast-like transitioning of vascular smooth muscle cells (VSMC) and endothelial cells (EC) was quantified using immunofluorescent microscopy.

Results

Perivascular fibrosis was elevated in acute-phase (77.69 %) and subacute-phase (72.19 %: border zone 95.18 %: infarct core) MI patients (p < 0.0001) compared to controls (61.03 %). FAP expression was higher in both acute-phase (1.46 %) and subacute-phase (18.01 %: border zone 5.67 %: infarct core) compared to controls (0.46 %) (p < 0.05). VSMC fibroblast-like cellular transition (SMA + S100A4+ vessels fraction) was higher in acute-phase (31.96 %) and subacute-phase (21.90 %: border zone; 37.25 %: infarct core) MI compared to controls (8.95 %) (p < 0.05). Similarly, EC fibroblast-like cellular transition (CD31 + S100A4+ area fraction) was increased in acute-phase MI (10.14 %) and subacute-phase MI (8.31 %: border zone 10.15 %: infarct core) compared to controls (2.67 %) (p < 0.05).

Conclusion

Increased perivascular fibrosis, fibroblast activation and vascular cellular transition in intramyocardial blood vessels of MI patients may contribute to MI development. Further increases of FAP expression and perivascular fibrosis, particularly in subacute-phase infarct cores, suggest MI itself exacerbates fibroblast activation and perivascular fibrosis, theoretically increasing reinfarction risk.

背景和目的：心肌微循环的结构和功能改变增加心肌梗死（MI）的风险。本研究通过对急性和亚急性心肌梗死死亡患者心肌内血管周围纤维化和前纤维化细胞转移的研究，探讨其在心肌梗死发病机制中的作用。方法：在心肌梗死急性期(3 ~ 6 h；n = 24)，亚急性期MI(5-14天；N = 12)和非梗死对照组（N = 14）。采用免疫组化方法定量测定血管周围纤维化和成纤维细胞活化蛋白（FAP）的表达。应用免疫荧光显微镜定量观察血管平滑肌细胞（VSMC）和内皮细胞（EC）的成纤维样转化。结果：心肌梗死急性期（77.69%）和亚急性期（72.19%：交界区95.18%：梗死核心）患者血管周围纤维化升高（p p p p）。结论：心肌梗死患者心肌血管血管周围纤维化、成纤维细胞活化和血管细胞转化的增加可能与心肌梗死的发展有关。FAP表达和血管周围纤维化的进一步增加，特别是在亚急性期梗死核心，表明心肌梗死本身加剧了成纤维细胞活化和血管周围纤维化，理论上增加了再梗死的风险。

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引用次数: 0

Sex steroid hormones and atrial electrophysiology: Vive la difference! 性类固醇激素与心房电生理：差异万岁！

Journal of molecular and cellular cardiology plus

Pub Date : 2024-12-01 DOI: 10.1016/j.jmccpl.2024.100087

Elise S. Bisset , Susan E. Howlett

引用次数: 0

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