Nature cardiovascular research最新文献_第3页

Spatially guided in vivo single-cell functional genomics of postnatal heart 空间引导出生后心脏的体内单细胞功能基因组学。

IF 12.6

Nature cardiovascular research Pub Date : 2026-09-07 DOI: 10.1038/s44161-026-00861-z

Haofei Wang, Yanhan Dong, Yiran Song, Marazzano Colon, Casey Grosso, Nicholas Yapundich, Shea Ricketts, Xingyan Liu, Gregory Farber, Smin L. Liu, Yunzhe Qian, Li Qian, Jiandong Liu

{"title":"Spatially guided in vivo single-cell functional genomics of postnatal heart","authors":"Haofei Wang, Yanhan Dong, Yiran Song, Marazzano Colon, Casey Grosso, Nicholas Yapundich, Shea Ricketts, Xingyan Liu, Gregory Farber, Smin L. Liu, Yunzhe Qian, Li Qian, Jiandong Liu","doi":"10.1038/s44161-026-00861-z","DOIUrl":"10.1038/s44161-026-00861-z","url":null,"abstract":"Understanding how spatial organization and cell−cell interactions shape gene regulatory programs is central to decoding tissue development and function. The transition at birth, marked by increased circulatory demands and rapid tissue growth, requires precise spatiotemporal coordination of cardiac maturation. In this study, we generated a high-resolution spatial and temporal atlas of the postnatal mouse heart by integrating single-nucleus RNA sequencing with image-based spatial transcriptomics. This framework revealed dynamic cellular interactions, niche-specific signaling and transcriptional programs guiding cardiomyocyte maturation. To functionally test prioritized regulators in vivo and at scale, we developed PIP-seq (probe-based indel-detectable Perturb-seq), a high-throughput platform that detects single guide RNA identity, infers gene editing and profiles transcription from fixed nuclei. Applying PIP-seq to the developing postnatal heart, we identified 21 previously uncharacterized regulators of cardiomyocyte maturation, including genes essential for sarcomere assembly, metabolic reprogramming and electrophysiological transitions. Together, our findings define how microenvironmental signals and intrinsic gene programs cooperate to guide heart maturation and establish a broadly applicable framework for functional genomics in complex tissues. By integrating single-nucleus RNA sequencing and spatial transcriptomics, Wang, Dong, Song et al. generated a high-resolution spatiotemporal atlas of the postnatal mouse heart, identifying 21 regulators of cardiomyocyte maturation and a spatially coordinated regulatory network underlying heart development.","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"5 9","pages":"848-868"},"PeriodicalIF":12.6,"publicationDate":"2026-09-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s44161-026-00861-z.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148907240","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Lifestyle and genetics modulate clonal hematopoiesis 生活方式和遗传调节克隆造血。

IF 12.6

Nature cardiovascular research Pub Date : 2026-09-03 DOI: 10.1038/s44161-026-00878-4

Vesna Todorovic

引用次数: 0

Genetic evidence supports the combined targeting of lipoprotein(a) and LDL cholesterol to reduce coronary artery disease risk 遗传证据支持脂蛋白(a)和低密度脂蛋白胆固醇联合靶向降低冠状动脉疾病风险。

IF 12.6

Nature cardiovascular research Pub Date : 2026-09-03 DOI: 10.1038/s44161-026-00865-9

Shaoqi Wang, Yuzhong Tang, Yang Sui, Hongqiang Zhao, Asifullah Khan, Wanqing Yin, Qiuli Chen, Tingfeng Xu, Zhaoqi Liu, Zhang Zhang, Fei Wang, Shuangli Mi, Kelvin Supriami, Min Seo Kim, Yuan Zhou, Hongjie Shi, Xudong Xing, Ying Yang, Yajing Hao, Jianping Li, Jie Du, Chenglong Yu, Sarah Urbut, Michael C. Honigberg, Pradeep Natarajan, JinPing Liu, Akl C. Fahed, Minxian Wang

{"title":"Genetic evidence supports the combined targeting of lipoprotein(a) and LDL cholesterol to reduce coronary artery disease risk","authors":"Shaoqi Wang, Yuzhong Tang, Yang Sui, Hongqiang Zhao, Asifullah Khan, Wanqing Yin, Qiuli Chen, Tingfeng Xu, Zhaoqi Liu, Zhang Zhang, Fei Wang, Shuangli Mi, Kelvin Supriami, Min Seo Kim, Yuan Zhou, Hongjie Shi, Xudong Xing, Ying Yang, Yajing Hao, Jianping Li, Jie Du, Chenglong Yu, Sarah Urbut, Michael C. Honigberg, Pradeep Natarajan, JinPing Liu, Akl C. Fahed, Minxian Wang","doi":"10.1038/s44161-026-00865-9","DOIUrl":"10.1038/s44161-026-00865-9","url":null,"abstract":"Distinct genetic mechanisms govern how lipoprotein(a) (Lp(a)) and low-density lipoprotein cholesterol (LDL-C) promote atherosclerosis. It remains unclear whether targeting both provides additive cardiovascular benefits. Here we use coding loss-of-function variants in LPA and PCSK9 and genetic scores associated with Lp(a) and LDL-C levels to evaluate the effects of lowering Lp(a) and LDL-C on coronary artery disease (CAD) risk. Among 408,039 individuals from the UK Biobank, LPA or PCSK9 loss-of-function carriers have lower CAD risk than noncarriers (odds ratio (OR) 0.91 and 0.81). Carriers of both variants have even lower CAD risk (OR 0.73). Genetic lowering of Lp(a) and LDL-C showed a stronger reduction of CAD risk (OR 0.70) than either trait individually (OR 0.85 and 0.81) in the two-factor genetic score analysis. Among statin users, Lp(a) reduction was linearly associated with CAD risk. A phenome-wide association study revealed that combined therapy was associated with cardiometabolic benefits without adverse effects. The additive benefits were replicated in 65,171 individuals from the Mass General Brigham Biobank. Wang et al. reveal that the genetic loss of LPA and PCSK9 results in additive cardiovascular risk reductions, supporting the combination of lipoprotein(a)- and low-density lipoprotein cholesterol-reducing agents in the clinic.","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"5 9","pages":"835-847"},"PeriodicalIF":12.6,"publicationDate":"2026-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148889713","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

A multiancestry polygenic risk score improves stratification in patients with hypertrophic cardiomyopathy 多祖先多基因风险评分改善肥厚性心肌病患者的分层。

IF 12.6

Nature cardiovascular research Pub Date : 2026-09-01 DOI: 10.1038/s44161-026-00866-8

Harshvir S. Bal, Akhil Pampana, Amrita Nayak, Mokshad Gaonkar, Sahaj Patel, Krishin Yerabolu, Nehal Vekariya, Nirav Patel, Rajat Kalra, Peng Li, Garima Arora, Pankaj Arora

{"title":"A multiancestry polygenic risk score improves stratification in patients with hypertrophic cardiomyopathy","authors":"Harshvir S. Bal, Akhil Pampana, Amrita Nayak, Mokshad Gaonkar, Sahaj Patel, Krishin Yerabolu, Nehal Vekariya, Nirav Patel, Rajat Kalra, Peng Li, Garima Arora, Pankaj Arora","doi":"10.1038/s44161-026-00866-8","DOIUrl":"10.1038/s44161-026-00866-8","url":null,"abstract":"Hypertrophic cardiomyopathy (HCM) has traditionally been considered a Mendelian disease driven by pathogenic or likely pathogenic variants in sarcomere-encoding genes (SARC-HCM-P/LP). However, these variants explain only one-third of cases, and variable penetrance suggests additional polygenic contributions. Existing HCM polygenic risk scores (PRSs), largely derived from European-ancestry cohorts, have limited generalizability. Here we develop a multiancestry PRS using summary statistics from the BioBank Japan, Million Veteran Program and a meta-analysis of seven European-ancestry cohorts and evaluate its association with HCM in a USA-based multiancestry population. Individuals with the highest PRS quintile had a 2.11-fold increased risk of HCM in the overall population and nearly 70-fold higher risk among SARC-HCM-P/LP carriers. The PRS improved risk stratification and showed trends toward improved ancestry-specific prediction. Among individuals with HCM, a higher PRS was also associated with adverse cardiovascular outcomes. These findings support the integration of multiancestry PRSs into HCM risk assessment and prognostication. Bal et al. develop a multiancestry polygenic risk score for hypertrophic cardiomyopathy and demonstrate its association with the disease in a heterogeneous national population.","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"5 9","pages":"891-903"},"PeriodicalIF":12.6,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148876890","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

Psychological stress impairs hematopoietic stem cell function through a brain–gut–bone marrow axis 心理压力通过脑-肠-骨髓轴损害造血干细胞功能。

IF 12.6

Nature cardiovascular research Pub Date : 2026-08-31 DOI: 10.1038/s44161-026-00879-3

Andrea Tavosanis

引用次数: 0

ALPK3 gene addition to restore sarcomeric quality control 添加ALPK3基因恢复肌体质量控制。

IF 12.6

Nature cardiovascular research Pub Date : 2026-08-31 DOI: 10.1038/s44161-026-00867-7

Julian Grünewald, Christian Kupatt

引用次数: 0

Author Correction: Endothelial IGFBP6 suppresses vascular inflammation and atherosclerosis 作者更正：内皮IGFBP6抑制血管炎症和动脉粥样硬化。

IF 12.6

Nature cardiovascular research Pub Date : 2026-08-27 DOI: 10.1038/s44161-026-00876-6

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

引用次数: 0

Author Correction: The TRPM7 chanzyme in smooth muscle cells drives abdominal aortic aneurysm in mice 作者更正：平滑肌细胞中的TRPM7酶驱动小鼠腹主动脉瘤。

IF 12.6

Nature cardiovascular research Pub Date : 2026-08-25 DOI: 10.1038/s44161-026-00877-5

Xuan Wang, Mi Wang, Tian-Tian Zhu, Zi-Jie Zheng, Shuang Li, Zhao-Yi Sui, Xin Guo, Sha Wu, Nai-Ning Zhang, Zhi-Yi Yu, Chang-Ping Hu, Yong-Bo Tang, Qing Wang, Zheng Zhang

引用次数: 0

The neglected role of lethal arrhythmia in the sudden death of stroke survivors 致命心律失常在中风幸存者猝死中被忽视的作用。

IF 12.6

Nature cardiovascular research Pub Date : 2026-08-25 DOI: 10.1038/s44161-026-00868-6

Vishnu Kadiyala, Kyndaron Reinier, Sumeet S. Chugh

引用次数: 0

Bridging clinical and experimental research to unravel mechanisms of the cardiovascular–kidney–metabolic syndrome 衔接临床与实验研究，揭示心肾代谢综合征的机制。

IF 12.6

Nature cardiovascular research Pub Date : 2026-08-20 DOI: 10.1038/s44161-026-00863-x

Katherine R. Tuttle

引用次数: 0