Nature cardiovascular research最新文献

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Norepinephrine oscillations regulate glymphatic clearance during spleen 去甲肾上腺素振荡调节脾脏过程中的甘油清除。

IF 9.4 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS

Nature cardiovascular research

Pub Date : 2025-02-04 DOI: 10.1038/s44161-025-00616-2

Elisa Martini

引用次数: 0

Specialized NK T cells protect the brain from injury after cardiac arrest 特化的 NK T 细胞能在心脏骤停后保护大脑免受损伤。

IF 9.4 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS

Nature cardiovascular research

Pub Date : 2025-01-31 DOI: 10.1038/s44161-025-00614-4

Andrea Tavosanis

引用次数: 0

Implications and limitations of the CLEAR-SYNERGY trial for the use of low-dose colchicine in cardiovascular disease.

IF 9.4 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS

Nature cardiovascular research

Pub Date : 2025-01-24 DOI: 10.1038/s44161-024-00600-2

Ashish Misra, Peter J Psaltis, Amandeep Rashid Mondal, Adam J Nelson, Stefan Mark Nidorf

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Mitochondrial NAD⁺ transporter SLC25A51 linked to human aortic disease.

IF 9.4 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS

Nature cardiovascular research

Pub Date : 2025-01-22 DOI: 10.1038/s44161-024-00599-6

Gabriel K Adzika, Ricardo A Velázquez Aponte, Joseph A Baur

引用次数: 0

Discovering and targeting mitochondrial loss in NOTCH1-related aortic aneurysm

IF 9.4 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS

Nature cardiovascular research

Pub Date : 2025-01-22 DOI: 10.1038/s44161-025-00607-3

We established a mouse model of progressive aortic aneurysm induced by conditional Notch1 deficiency in vascular smooth muscle cells. Notch1 deficiency impairs the transcription of genes involved in mitochondrial fusion and biogenesis, thereby triggering aortic pathology. Early intervention to enhance these mitochondrial processes could potentially slow disease progression.

引用次数: 0

Mitochondrial NAD⁺ deficiency in vascular smooth muscle impairs collagen III turnover to trigger thoracic and abdominal aortic aneurysm.

IF 9.4 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS

Nature cardiovascular research

Pub Date : 2025-01-22 DOI: 10.1038/s44161-024-00606-w

Jingjing Zhang, Yuyi Tang, Shan Zhang, Zhuxin Xie, Wenrui Ma, Shaowen Liu, Yixuan Fang, Shufen Zheng, Ce Huang, Guoquan Yan, Mieradilijiang Abudupataer, Yue Xin, Jingqiao Zhu, Wenjing Han, Weizhong Wang, Fenglin Shen, Hao Lai, Yang Liu, Dan Ye, Fa-Xing Yu, Yanhui Xu, Cuiping Pan, Chunsheng Wang, Kai Zhu, Weijia Zhang

Thoracic and abdominal aortic aneurysm poses a substantial mortality risk in adults, yet many of its underlying factors remain unidentified. Here, we identify mitochondrial nicotinamide adenine dinucleotide (NAD)⁺ deficiency as a causal factor for the development of aortic aneurysm. Multiomics analysis of 150 surgical aortic specimens indicated impaired NAD⁺ salvage and mitochondrial transport in human thoracic aortic aneurysm, with expression of the NAD⁺ transporter SLC25A51 inversely correlating with disease severity and postoperative progression. Genome-wide gene-based association analysis further linked low SLC25A51 expression to risk of aortic aneurysm and dissection. In mouse models, smooth muscle-specific knockout of Nampt, Nmnat1, Nmnat3, Slc25a51, Nadk2 and Aldh18a1, genes involved in NAD⁺ salvage and transport, induced aortic aneurysm, with Slc25a51 deletion producing the most severe effects. Using these models, we suggest a mechanism that may explain the disease pathogenesis: the production of type III procollagen during aortic medial matrix turnover imposes a high demand for proline, an essential amino acid component of collagen. Deficiency in the mitochondrial NAD⁺ pool, regulated by NAD⁺ salvage and transport, hinders proline biosynthesis in mitochondria, contributing to thoracic and abdominal aortic aneurysm.

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引用次数: 0

The clinical promise of 18F-flurpiridaz PET imaging heralds a new frontier in the diagnosis and management of coronary artery disease 18F-flurpiridaz PET成像的临床前景预示着冠状动脉疾病诊断和治疗的新前沿

IF 9.4 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS

Nature cardiovascular research

Pub Date : 2025-01-17 DOI: 10.1038/s44161-024-00587-w

René R. Sevag Packard

The PET radiotracer 18F-flurpiridaz has undergone rigorous clinical testing and gained FDA approval for the evaluation of coronary artery disease. Its unique properties suggest 18F-flurpiridaz has the potential to transform the field of nuclear myocardial perfusion imaging and blood flow quantification, with far-reaching effects on cardiovascular care.

PET示踪剂18F-flurpiridaz经过了严格的临床测试，并获得了FDA批准用于评估冠状动脉疾病。其独特的性质表明，18f -氟吡达兹有可能改变核心肌灌注成像和血流量化领域，对心血管保健产生深远的影响。

引用次数: 0

The highly conserved PIWI-interacting RNA CRAPIR antagonizes PA2G4-mediated NF110–NF45 disassembly to promote heart regeneration in mice 高度保守的piwi相互作用RNA CRAPIR可拮抗pa2g4介导的NF110-NF45分解，促进小鼠心脏再生

IF 9.4 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS

Nature cardiovascular research

Pub Date : 2025-01-15 DOI: 10.1038/s44161-024-00592-z

Wenya Ma, Hongyang Chen, Yanan Tian, Wei Huang, Zhongyu Ren, Jianglong Li, Qimeng Ouyang, Yu Hu, Xin Wang, Haoyu Ji, Xu Liu, Yu Liu, XiuXiu Wang, Yining Liu, Ye Tian, Faqian Li, Baofeng Yang, Ning Wang, Benzhi Cai

Targeting the cardiomyocyte cell cycle is a promising strategy for heart repair following injury. Here, we identify a cardiac-regeneration-associated PIWI-interacting RNA (CRAPIR) as a regulator of cardiomyocyte proliferation. Genetic ablation or antagomir-mediated knockdown of CRAPIR in mice impairs cardiomyocyte proliferation and reduces heart regenerative potential. Conversely, overexpression of CRAPIR promotes cardiomyocyte proliferation, reduces infarct size and improves heart function after myocardial infarction. Mechanistically, CRAPIR promotes cardiomyocyte proliferation by competing with NF110 for binding to the RNA-binding protein PA2G4, thereby preventing the interaction of PA2G4 with the NF110–NF45 heterodimer and reducing NF110 degradation. The ability of CRAPIR to promote proliferation was confirmed in human embryonic stem cell-derived cardiomyocytes. Notably, CRAPIR serum levels are lower in individuals with ischemic heart disease and negatively correlate with levels of N-terminal pro-brain natriuretic peptide. These findings position CRAPIR both as a potential diagnostic marker for cardiac injury and as a therapeutic target for heart regeneration through the PA2G4–NF110–NF45 signaling axis. Ma et al. identify a highly conserved PIWI-interacting RNA CRAPIR, as a key regulator of cardiomyocyte proliferation and heart repair after myocardial infarction through the PA2G4–NF110–NF45 signaling axis.

靶向心肌细胞周期是一种很有前途的心脏损伤修复策略。在这里，我们确定了心脏再生相关的piwi相互作用RNA （CRAPIR）作为心肌细胞增殖的调节因子。基因消融或安他哥莫介导的小鼠CRAPIR的下调会损害心肌细胞增殖并降低心脏再生潜能。相反，CRAPIR过表达可促进心肌细胞增殖，减少梗死面积，改善心肌梗死后心功能。从机制上讲，CRAPIR通过与NF110竞争结合rna结合蛋白PA2G4来促进心肌细胞增殖，从而阻止PA2G4与NF110 - nf45异源二聚体的相互作用，减少NF110的降解。在人胚胎干细胞来源的心肌细胞中证实了CRAPIR促进增殖的能力。值得注意的是，缺血性心脏病患者的CRAPIR血清水平较低，并与n端脑利钠肽前体水平呈负相关。这些发现将CRAPIR定位为心脏损伤的潜在诊断标志物，并通过PA2G4-NF110-NF45信号轴作为心脏再生的治疗靶点。Ma等人发现一种高度保守的piwi相互作用RNA CRAPIR，通过PA2G4-NF110-NF45信号轴，作为心肌细胞增殖和心肌梗死后心脏修复的关键调节因子。

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引用次数: 0

Powering up piRNAs for heart regeneration 为心脏再生激活pirna

IF 9.4 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS

Nature cardiovascular research

Pub Date : 2025-01-15 DOI: 10.1038/s44161-024-00590-1

Thierry Pedrazzini

Heart regeneration after tissue injury depends on the proliferation of existing cardiomyocytes. Manipulating the non-coding transcriptome holds promise for the therapeutic induction of cardiomyocyte proliferation in the damaged human heart. A study now demonstrates that piRNAs have key roles in this regenerative process.

组织损伤后的心脏再生依赖于现有心肌细胞的增殖。操纵非编码转录组有望在受损的人类心脏中治疗性诱导心肌细胞增殖。现在的一项研究表明，pirna在这一再生过程中起着关键作用。

引用次数: 0

Correcting mitochondrial loss mitigates NOTCH1-related aortopathy in mice 纠正线粒体丢失可减轻小鼠notch1相关主动脉病变。

IF 9.4 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS

Nature cardiovascular research

Pub Date : 2025-01-14 DOI: 10.1038/s44161-024-00603-z

Yuyi Tang, Jingjing Zhang, Yixuan Fang, Kai Zhu, Jingqiao Zhu, Ce Huang, Zhuxin Xie, Shan Zhang, Wenrui Ma, Guoquan Yan, Shaowen Liu, Xin Liu, Wenjing Han, Yue Xin, Chenxi Yang, Mieradilijiang Abudupataer, Peiyun Zhou, Chenxi He, Hao Lai, Chunsheng Wang, Yang Liu, Fei Lan, Dan Ye, Fa-Xing Yu, Yanhui Xu, Weijia Zhang

Loss-of-function mutations in NOTCH1 were previously linked to thoracic aortopathy, a condition for which non-surgical treatment options are limited. Based on clinical proteome analysis, we hypothesized that mitochondrial fusion and biogenesis in aortic smooth muscle cells (SMCs) are crucial for regulating the progression of NOTCH1-related aortopathy. Here we demonstrate that SMC-specific Notch1 knockout mice develop aortic pathology, including stiffening, dilation and focal dissection. These changes are accompanied by decreased expression of MFN1/2 and TFAM, mirroring findings in human patients. SMC-specific deletion of Mfn1 and/or Mfn2 genes recapitulates the aortopathy seen in Notch1-deficient mice. Prophylactic or therapeutic approaches aimed at increasing mitochondrial DNA copy number, either through AAV-mediated overexpression of Mfn1/2 or oral treatment with mitofusion activators teriflunomide or leflunomide, help mitigate or slow the progression of aortopathy in SMC-Notch1−/− mice. Our findings provide a molecular framework for exploring pharmacological interventions to restore mitochondrial function in NOTCH1-related aortopathy. Tang, Zhang, Fang, Zhu et al. identify impaired mitochondrial fusion and biogenesis as a key mechanism underlying NOTCH1-associated aortic pathology and show that correcting mitochondrial loss in mutant mice using repurposed drugs teriflunomide or leflunomide slows the progression of aoropathy.

NOTCH1的功能缺失突变先前与胸主动脉病变有关，这是一种非手术治疗选择有限的疾病。基于临床蛋白质组学分析，我们假设主动脉平滑肌细胞（SMCs）的线粒体融合和生物发生对于调节notch1相关主动脉病变的进展至关重要。在这里，我们证明了smc特异性Notch1敲除小鼠出现主动脉病理，包括硬化、扩张和局灶性夹层。这些变化伴随着MFN1/2和TFAM的表达降低，与人类患者的发现相一致。smc特异性的Mfn1和/或Mfn2基因缺失再现了notch1缺陷小鼠的主动脉病变。通过aav介导的Mfn1/2过表达或口服线粒体融合激活剂teri氟米特或来氟米特，旨在增加线粒体DNA拷贝数的预防性或治疗性方法有助于减轻或减缓SMC-Notch1-/-小鼠主动脉病变的进展。我们的研究结果为探索药物干预恢复notch1相关主动脉病变的线粒体功能提供了一个分子框架。

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