Nature cardiovascular research最新文献

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

IF 9.4

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

引用次数: 0

Mitochondrial NAD⁺ transporter SLC25A51 linked to human aortic disease.

IF 9.4

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

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

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

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

{"title":"Mitochondrial NAD+ deficiency in vascular smooth muscle impairs collagen III turnover to trigger thoracic and abdominal aortic aneurysm.","authors":"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","doi":"10.1038/s44161-024-00606-w","DOIUrl":"https://doi.org/10.1038/s44161-024-00606-w","url":null,"abstract":"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.","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":" ","pages":""},"PeriodicalIF":9.4,"publicationDate":"2025-01-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143026210","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

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

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

René R. Sevag Packard

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

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

{"title":"The highly conserved PIWI-interacting RNA CRAPIR antagonizes PA2G4-mediated NF110–NF45 disassembly to promote heart regeneration in mice","authors":"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","doi":"10.1038/s44161-024-00592-z","DOIUrl":"10.1038/s44161-024-00592-z","url":null,"abstract":"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.","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"4 1","pages":"102-118"},"PeriodicalIF":9.4,"publicationDate":"2025-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142995883","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

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

IF 9.4

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

Thierry Pedrazzini

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

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

{"title":"Correcting mitochondrial loss mitigates NOTCH1-related aortopathy in mice.","authors":"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","doi":"10.1038/s44161-024-00603-z","DOIUrl":"10.1038/s44161-024-00603-z","url":null,"abstract":"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.","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":" ","pages":""},"PeriodicalIF":9.4,"publicationDate":"2025-01-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142985656","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

IGFBP6 contributes to vascular resilience. IGFBP6有助于血管恢复。

IF 9.4

Nature cardiovascular research Pub Date : 2025-01-10 DOI: 10.1038/s44161-024-00597-8

Martin A Schwartz

引用次数: 0

Endothelial IGFBP6 suppresses vascular inflammation and atherosclerosis. 内皮IGFBP6抑制血管炎症和动脉粥样硬化。

IF 9.4

Nature cardiovascular research Pub Date : 2025-01-10 DOI: 10.1038/s44161-024-00591-0

Meiming Su, Wenqi Zhao, Hui Jiang, Yaping Zhao, Zhaopeng Liao, Zhenghong Liu, Mengyun Xu, Shanshan Jiang, Lili Wu, Yi Yang, Zhihua Wang, Zhutian Zeng, Yun Fang, Chaojun Tang, Clint L Miller, Paul C Evans, Li Wang, Maciej Banach, Hanjoong Jo, Bradford C Berk, Stefan Offermanns, Yu Huang, Junbo Ge, Suowen Xu, Jianping Weng

{"title":"Endothelial IGFBP6 suppresses vascular inflammation and atherosclerosis.","authors":"Meiming Su, Wenqi Zhao, Hui Jiang, Yaping Zhao, Zhaopeng Liao, Zhenghong Liu, Mengyun Xu, Shanshan Jiang, Lili Wu, Yi Yang, Zhihua Wang, Zhutian Zeng, Yun Fang, Chaojun Tang, Clint L Miller, Paul C Evans, Li Wang, Maciej Banach, Hanjoong Jo, Bradford C Berk, Stefan Offermanns, Yu Huang, Junbo Ge, Suowen Xu, Jianping Weng","doi":"10.1038/s44161-024-00591-0","DOIUrl":"10.1038/s44161-024-00591-0","url":null,"abstract":"Beyond dyslipidemia, inflammation contributes to the development of atherosclerosis. However, intrinsic factors that counteract vascular inflammation and atherosclerosis remain scarce. Here we identify insulin-like growth factor binding protein 6 (IGFBP6) as a homeostasis-associated molecule that restrains endothelial inflammation and atherosclerosis. IGFBP6 levels are significantly reduced in human atherosclerotic arteries and patient serum. Reduction of IGFBP6 in human endothelial cells by siRNA increases inflammatory molecule expression and monocyte adhesion. Conversely, pro-inflammatory effects mediated by disturbed flow (DF) and tumor necrosis factor (TNF) are reversed by IGFBP6 overexpression. Mechanistic investigations further reveal that IGFBP6 executes anti-inflammatory effects directly through the major vault protein (MVP)-c-Jun N-terminal kinase (JNK)/nuclear factor kappa B (NF-κB) signaling axis. Finally, IGFBP6-deficient mice show aggravated diet- and DF-induced atherosclerosis, whereas endothelial-cell-specific IGFBP6-overexpressing mice protect against atherosclerosis. Based on these findings, we propose that reduction of endothelial IGFBP6 is a predisposing factor in vascular inflammation and atherosclerosis, which can be therapeutically targeted.","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":" ","pages":""},"PeriodicalIF":9.4,"publicationDate":"2025-01-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142967602","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0