Nature cardiovascular research最新文献_第8页

Consensus statement on mass spectrometry-based proteomic analysis of cardiac tissue 基于质谱的心脏组织蛋白质组学分析的共识声明。

IF 12.6

Nature cardiovascular research Pub Date : 2026-05-25 DOI: 10.1038/s44161-026-00824-4

Alicia Lundby, Jennifer E. Van Eyk, Manuel Mayr, Melanie Y. White, Jonathan A. Kirk, Jonathan S. Achter, Justyna Fert-Bober, Michael Wierer, Philipp Mertins, Maggie P. Y. Lam, Sean J. Humphrey, Edward Lau, Anthony O. Gramolini, Ying Ge, Rebekah L. Gundry

{"title":"Consensus statement on mass spectrometry-based proteomic analysis of cardiac tissue","authors":"Alicia Lundby, Jennifer E. Van Eyk, Manuel Mayr, Melanie Y. White, Jonathan A. Kirk, Jonathan S. Achter, Justyna Fert-Bober, Michael Wierer, Philipp Mertins, Maggie P. Y. Lam, Sean J. Humphrey, Edward Lau, Anthony O. Gramolini, Ying Ge, Rebekah L. Gundry","doi":"10.1038/s44161-026-00824-4","DOIUrl":"10.1038/s44161-026-00824-4","url":null,"abstract":"Mass spectrometry-based cardiac proteomics provides direct molecular insight into cardiac physiology and disease. While plasma proteomics has advanced biomarker discovery, the analysis of cardiac tissue is essential for mechanistic understanding and therapeutic target identification; however, proteomic investigation of cardiac tissue faces unique challenges, including limited sample availability, regional heterogeneity, variability in collection and processing, and inconsistent reporting practices that hinder reproducibility and data integration. Here, we provide a practical framework for designing and conducting mass spectrometry-based proteomic studies of cardiac tissue and primary cardiac cells. We outline best practices and key considerations for sample handling, experimental design, data acquisition, quality control and statistical analysis. This guideline aims to support cardiac researchers in generating robust and reproducible proteomics datasets that advance our understanding of cardiac biology in both physiological and pathological contexts. This Consensus Statement provides practical guidance for mass spectrometry-based proteomic analyses of cardiac tissue samples. It defines best practices across the experimental workflow to enable reproducible, high-quality datasets.","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"5 6","pages":"526-540"},"PeriodicalIF":12.6,"publicationDate":"2026-05-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s44161-026-00824-4.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148019155","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

CAMK2 inhibition treats genetic dilated cardiomyopathy in mice CAMK2抑制对小鼠遗传性扩张型心肌病的治疗作用。

IF 12.6

Nature cardiovascular research Pub Date : 2026-05-21 DOI: 10.1038/s44161-026-00826-2

引用次数: 0

Single-cell and spatial transcriptomics identify immune–stromal interactions in cardiac allograft vasculopathy 单细胞和空间转录组学鉴定同种异体心脏移植血管病变中免疫-基质相互作用

IF 10.8

Nature cardiovascular research Pub Date : 2026-05-18 DOI: 10.1038/s44161-026-00813-7

Macee C. Owen, Daniel Yuhang Li, Haewon Shin, Wenduo Gu, Alekhya Parvathaneni, Farid F. Kadyrov, Xiaoran Wang, Maura Sticco-Ivins, Gianni Bonnici, Samantha L. Nelson, Hao Dun, Sariah Hyacinth, Samantha C. Giangrasso, Caroline Chou, Chieh-Yu Lin, Michael T. Cain, Albert Pedroza, Alex Dalal, Karim Sallam, Jack Boyd, Joseph Woo, Junedh M. Amrute, Paul Cheng, Kory J. Lavine, Benjamin J. Kopecky

{"title":"Single-cell and spatial transcriptomics identify immune–stromal interactions in cardiac allograft vasculopathy","authors":"Macee C. Owen, Daniel Yuhang Li, Haewon Shin, Wenduo Gu, Alekhya Parvathaneni, Farid F. Kadyrov, Xiaoran Wang, Maura Sticco-Ivins, Gianni Bonnici, Samantha L. Nelson, Hao Dun, Sariah Hyacinth, Samantha C. Giangrasso, Caroline Chou, Chieh-Yu Lin, Michael T. Cain, Albert Pedroza, Alex Dalal, Karim Sallam, Jack Boyd, Joseph Woo, Junedh M. Amrute, Paul Cheng, Kory J. Lavine, Benjamin J. Kopecky","doi":"10.1038/s44161-026-00813-7","DOIUrl":"10.1038/s44161-026-00813-7","url":null,"abstract":"Cardiac allograft vasculopathy (CAV) is the leading cause of mortality after heart transplantation, yet no targeted therapies exist to prevent or reverse disease progression, and patients with CAV ultimately require a retransplant. CAV is characterized by progressive neointimal hyperplasia in donor coronary arteries, resulting in luminal occlusion and eventual allograft failure. Although immune and stromal cell interactions are thought to drive disease, the key cellular and molecular mechanisms remain poorly defined. Here we integrate single-cell RNA sequencing and spatial transcriptomics of human coronary arteries to characterize the CAV neointimal microenvironment. By comparing arteries with CAV with atherosclerotic coronary artery disease and non-diseased controls, we identify a distinct transcriptional signature of CAV. Our analysis reveals that modulated vascular smooth muscle cells and macrophage subsets dominate the neointima and interact to promote type 1 interferon (IFN)-mediated inflammation. Using a mouse model of CAV, we show that IFN signaling blockade with ruxolitinib significantly reduces CAV incidence and prolongs allograft survival. These findings define key cellular drivers of CAV and highlight IFN signaling as a potential therapeutic target. Owen et al. used single-cell RNA sequencing and spatial transcriptomics to analyze graft cells in heart transplants with cardiac allograft vasculopathy, showing that vascular smooth muscle cells and macrophages drive interferon-mediated inflammation and that JAK signaling blockade prolongs allograft survival.","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"5 5","pages":"439-455"},"PeriodicalIF":10.8,"publicationDate":"2026-05-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147968211","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

Macrophages orchestrate the landscape of advanced cardiac allograft vasculopathy 巨噬细胞调控晚期异体心脏移植血管病变的景观

IF 10.8

Nature cardiovascular research Pub Date : 2026-05-18 DOI: 10.1038/s44161-026-00814-6

Eleni Tseliou, Stavros G. Drakos, Edward B. Thorp

引用次数: 0

Ischemic heart disease burden and healthcare system readiness across sub-Saharan Africa 撒哈拉以南非洲地区缺血性心脏病负担和卫生保健系统准备情况。

IF 10.8

Nature cardiovascular research Pub Date : 2026-05-13 DOI: 10.1038/s44161-026-00817-3

Mark P. Khurana, Johan S. Bundgaard, Kidola Jeremiah, Cody Cichowitz, Godfrey Kisigo, Grace Ruselu, Lily Yan, Maja V. Kragh, Rasmus Hasselbalch, Borja Ibáñez, George Praygod, Daniel Faurholt-Jepsen, Henning Bundgaard, Robert N. Peck

{"title":"Ischemic heart disease burden and healthcare system readiness across sub-Saharan Africa","authors":"Mark P. Khurana, Johan S. Bundgaard, Kidola Jeremiah, Cody Cichowitz, Godfrey Kisigo, Grace Ruselu, Lily Yan, Maja V. Kragh, Rasmus Hasselbalch, Borja Ibáñez, George Praygod, Daniel Faurholt-Jepsen, Henning Bundgaard, Robert N. Peck","doi":"10.1038/s44161-026-00817-3","DOIUrl":"10.1038/s44161-026-00817-3","url":null,"abstract":"Sub-Saharan Africa is experiencing a rapid rise in ischemic heart disease, creating new challenges for regional health systems. As populations grow and urbanize, lifestyle, metabolic, nutritional and environmental factors are reshaping the burden of noncommunicable diseases. Yet health systems, historically oriented toward communicable diseases and maternal health, show variable capacity to prevent, diagnose and treat ischemic heart disease. Despite increasing recognition, systematic assessments of country-level disease burden and healthcare capacity are limited, leaving gaps for evidence-based policy. Here we address this gap by assessing healthcare system readiness across four domains: health system capacities, primary care, secondary and tertiary care, and health system context. We highlight how limitations in workforce, essential medicines, diagnostics and policy intersect with upstream drivers such as obesity, hypertension, diabetes, smoking, dietary transitions, urbanization and environmental stressors. Meeting these challenges will require coordinated investment, equitable resource allocation and integrated prevention strategies. Khurana et al. share their perspective on healthcare system preparedness in sub-Saharan Africa in light of the recent increase in ischemic heart disease burden, highlighting areas that require intervention to improve the management of this noncommunicable condition in the region.","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"5 5","pages":"394-403"},"PeriodicalIF":10.8,"publicationDate":"2026-05-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147935639","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

CD98hc controls CNS angiogenesis and blood–brain barrier integrity through localized regulation of the systemic integrin–FAK pathway CD98hc通过局部调控系统整合素- fak通路控制中枢神经系统血管生成和血脑屏障完整性。

IF 10.8

Nature cardiovascular research Pub Date : 2026-05-12 DOI: 10.1038/s44161-026-00816-4

Xiaoyan Hu, Min Yu, Shilun Yang, Cheng Fang, Pengju Wei, Xun Zhang, Yinzhong Ma, Ziying Feng, Yukun Chen, Jingyu Yan, Ying Wang, Linhui Qiu, Dengpan Song, Fuyou Guo, Junlei Chang

{"title":"CD98hc controls CNS angiogenesis and blood–brain barrier integrity through localized regulation of the systemic integrin–FAK pathway","authors":"Xiaoyan Hu, Min Yu, Shilun Yang, Cheng Fang, Pengju Wei, Xun Zhang, Yinzhong Ma, Ziying Feng, Yukun Chen, Jingyu Yan, Ying Wang, Linhui Qiu, Dengpan Song, Fuyou Guo, Junlei Chang","doi":"10.1038/s44161-026-00816-4","DOIUrl":"10.1038/s44161-026-00816-4","url":null,"abstract":"Normal vascular structure and function are crucial for the homeostasis of the central nervous system (CNS), yet the regulation of CNS vasculature remains incompletely understood. Here we show that CD98 heavy chain (CD98hc), also known as SLC3A2 or 4F2hc, is essential for CNS angiogenesis and blood–brain barrier (BBB) integrity. CD98hc is selectively enriched in the CNS endothelium versus the peripheral endothelium in mice and humans. Ablation of endothelial CD98hc in mouse embryos leads to aberrant CNS angiogenesis, impaired BBB formation and cerebral hemorrhage, without affecting the peripheral vasculature. In adults, endothelial CD98hc deficiency does not impact homeostatic CNS angiogenesis but disrupts the BBB and causes neurological deficits. The mechanism involves a CNS-specific reduction in the systemic integrin–FAK pathway in endothelial cells, affecting subsequent VEGFR2 and Wnt–β-catenin pathways. Importantly, FAK activation fully rectifies the CNS vascular phenotype in CD98hc-deficient mice. These findings open promising avenues for CNS-specific vascular regulation and targeted therapy of cerebrovascular diseases. Hu et al. show that the transmembrane glycoprotein CD98hc in cerebral endothelial cells regulates the integrin–FAK signaling pathway, thereby promoting angiogenesis and maintaining blood–brain barrier integrity.","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"5 5","pages":"456-478"},"PeriodicalIF":10.8,"publicationDate":"2026-05-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147935630","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

Publisher Correction: The NPR1 agonist XXB750 may worsen heart failure 发布者更正：NPR1激动剂XXB750可能加重心力衰竭。

IF 10.8

Nature cardiovascular research Pub Date : 2026-05-11 DOI: 10.1038/s44161-026-00825-3

Andrea Tavosanis

引用次数: 0

Tolerogenic DCs expressing anti-FAP chimeric antigen receptor prevent adverse cardiac remodeling 表达抗fap嵌合抗原受体的耐受性dc可预防不良的心脏重构。

IF 10.8

Nature cardiovascular research Pub Date : 2026-05-07 DOI: 10.1038/s44161-026-00823-5

Elisa Martini

引用次数: 0

High-resolution cardiac mapping meets computational imaging to merge structure and function 高分辨率心脏测绘与计算机成像相结合，实现结构与功能的融合。

IF 10.8

Nature cardiovascular research Pub Date : 2026-05-05 DOI: 10.1038/s44161-026-00812-8

Bastiaan J. Boukens, Daniël A. Pijnappels

引用次数: 0

CAMK2D causes heart failure in mice with RBM20 cardiomyopathy CAMK2D引起RBM20心肌病小鼠心力衰竭。

IF 10.8

Nature cardiovascular research Pub Date : 2026-05-04 DOI: 10.1038/s44161-026-00818-2

Maarten M. G. van den Hoogenhof, Javier Duran, Thiago Britto-Borges, Vasco Sequeira, Elena Kemmling, Laura Konrad, Friederike Schreiter, David C. Lennermann, Joshua Hartmann, Laura Schraft, Julia Kornienko, Theresa Bock, Marcus Krüger, Christoph Maack, Christoph Dieterich, Lars M. Steinmetz, Matthias Dewenter, Johannes Backs

{"title":"CAMK2D causes heart failure in mice with RBM20 cardiomyopathy","authors":"Maarten M. G. van den Hoogenhof, Javier Duran, Thiago Britto-Borges, Vasco Sequeira, Elena Kemmling, Laura Konrad, Friederike Schreiter, David C. Lennermann, Joshua Hartmann, Laura Schraft, Julia Kornienko, Theresa Bock, Marcus Krüger, Christoph Maack, Christoph Dieterich, Lars M. Steinmetz, Matthias Dewenter, Johannes Backs","doi":"10.1038/s44161-026-00818-2","DOIUrl":"10.1038/s44161-026-00818-2","url":null,"abstract":"Although heart disease arises from different etiologies, treatment remains largely one-size-fits-all, leaving many patients without optimal benefit, which highlights the need for cause-directed therapies. Pathogenic variants in RBM20, a cardiac splicing factor, lead to an aggressive form of dilated cardiomyopathy with high risk of ventricular arrhythmias. We hypothesized that the splicing target calcium/calmodulin-dependent kinase II delta (CAMK2D) is disease causing in RBM20 cardiomyopathy. Here we show that Rbm20/Camk2d double knockout mice are protected from heart failure and sudden cardiac death. In Rbm20-deficient hearts, phosphorylation of CAMK2D targets was increased, indicating that RBM20 loss results not only in mis-splicing of Camk2d transcripts but also in functional activation of CAMK2D signaling. Reexpression of individual CAMK2D splice variants in Rbm20/Camk2d double knockout mice reintroduced cardiac dysfunction, demonstrating that overactivation, rather than mis-splicing, drives disease. Treatment of Rbm20-p.Arg636Gln knockin mice with the ATP-competitive CAMK2 inhibitor hesperadin improved cardiac function. These findings identify CAMK2D overactivation as a central mechanism in RBM20 cardiomyopathy and support CAMK2D inhibition as a promising cause-directed therapy. Pathogenic variants in RBM20 cause an aggressive form of heart disease. van den Hoogenhof et al. show that overactivated CAMK2D drives this disease, and that pharmacological CAMK2D inhibition is a promising therapeutic approach in patients with RBM20 cardiomyopathy.","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"5 5","pages":"479-491"},"PeriodicalIF":10.8,"publicationDate":"2026-05-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s44161-026-00818-2.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147847229","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