Nature cardiovascular research最新文献

{"title":"Collecting lymphatics unzip to drain injured lungs","authors":"Simon J. Cleary","doi":"10.1038/s44161-025-00682-6","DOIUrl":"10.1038/s44161-025-00682-6","url":null,"abstract":"Protease-activated receptor 1 (PAR1) allows platelets and blood endothelial cells to respond to coagulation. Research in mouse models has uncovered a new role for PAR1 — enabling pulmonary collecting lymphatics to transform their intercellular junctions from ‘zippers’ into ‘buttons’ for additional interstitial fluid drainage during acute lung injury.","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"4 8","pages":"959-961"},"PeriodicalIF":10.8,"publicationDate":"2025-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144661223","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}

{"title":"The thrombin receptor PAR1 orchestrates changes in lymphatic endothelial cell junction morphology to augment lymphatic drainage during lung injury","authors":"Chou Chou, Camila Ceballos Paredes, Barbara Summers, Jade Palmer-Johnson, Anjali Trivedi, Aneel Bhagwani, Kasper B. Hansen, Anders S. Kristensen, Stefka Gyoneva, Sharon A. Swanger, Stephen F. Traynelis, Hasina Outtz Reed","doi":"10.1038/s44161-025-00681-7","DOIUrl":"10.1038/s44161-025-00681-7","url":null,"abstract":"The lung lymphatic vasculature is capable of remarkable increases in lymphatic drainage in settings of inflammation and edema; however, the mechanisms driving this are not clear. Here we show that lung injury transforms the configuration of lung lymphatic endothelial cell junctions from a continuous ‘zippered’ configuration to a discontinuous and permeable ‘button’ configuration. Despite similarity to the junctional changes often seen in leaky and dysfunctional blood vessels, we find that the shift to button junctions in the lymphatic vasculature has an opposite effect, resulting in augmented lung lymphatic drainage. Mechanistically, we demonstrate that lung lymphatic button junction formation in models of lung injury is dependent on the thrombin receptor protease-activated receptor 1, a known mediator of blood vessel permeability. These results uncover a previously unknown role for the thrombin receptor protease-activated receptor 1 in the lymphatic vasculature that promotes a similar change in junction morphology as seen in blood vessels, but with a disparate effect on lymphatic function. Chou et al. demonstrate that activation of the thrombin receptor protease-activated receptor 1 in the lung lymphatic vasculature mediates morphological changes in lymphatic endothelial cell junctions to augment lung lymphatic drainage in models of lung injury.","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"4 8","pages":"964-975"},"PeriodicalIF":10.8,"publicationDate":"2025-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12343296/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144661224","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}

{"title":"A novel metabolic–epigenetic axis regulates vascular recovery","authors":"","doi":"10.1038/s44161-025-00674-6","DOIUrl":"10.1038/s44161-025-00674-6","url":null,"abstract":"We demonstrate a clear regulatory role for O-GlcNAcylation in cellular reprogramming and uncover potential molecular pathways conducive to enhancing perfusion restoration in ischemic tissue. These findings offer a promising avenue for the development of novel therapeutic interventions targeting vascular ischemia.","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"4 7","pages":"797-798"},"PeriodicalIF":10.8,"publicationDate":"2025-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144644320","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}

{"title":"Premenstrual disorders and risk of cardiovascular diseases","authors":"Yihui Yang, Emma Bränn, Jing Zhou, Dang Wei, Jacob Bergstedt, Fang Fang, Unnur A. Valdimarsdóttir, Elizabeth Bertone-Johnson, Donghao Lu","doi":"10.1038/s44161-025-00684-4","DOIUrl":"10.1038/s44161-025-00684-4","url":null,"abstract":"Several lines of evidence indicate a potential link between premenstrual disorders (PMDs) and cardiovascular diseases (CVDs). However, it remains unclear whether women with PMDs have a higher risk of CVDs. Here we present a Swedish nationwide population-based matched cohort study from 2001 to 2022 and a sibling matched cohort to address familial confounding. A total of 99,411 women with PMDs were included in the population analysis and 36,061 women with PMDs in the sibling analysis. Compared with individuals without PMDs, women with PMDs had a higher risk of any CVD (adjusted hazard ratio = 1.11 (95% confidence interval: 1.08–1.13) in the population analysis and 1.10 (95% confidence interval: 1.06–1.15) in the sibling analysis). The risk was particularly pronounced for PMDs diagnosed before 25 years of age and PMDs with comorbid perinatal depression. Our study shows that women who received a PMD diagnosis in specialist or primary care are at a higher risk of CVDs. Yang et al. draw evidence from population-based and sibling cohort studies to reveal that women suffering from premenstrual disorders are at an increased risk of cardiovascular disease.","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"4 8","pages":"1001-1010"},"PeriodicalIF":10.8,"publicationDate":"2025-07-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12343293/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144621445","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}

{"title":"Agonistic immune checkpoint regulator may harm the heart","authors":"","doi":"10.1038/s44161-025-00654-w","DOIUrl":"10.1038/s44161-025-00654-w","url":null,"abstract":"The use of cancer immunotherapies is expanding to patients resistant to current therapies, and emerging regulators of immune checkpoints such as agonist antibodies that directly activate immune responses are being studied. Although these therapeutics are promising, this study highlights the potential for cardiac immune-related adverse events.","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"4 7","pages":"799-800"},"PeriodicalIF":10.8,"publicationDate":"2025-07-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144602413","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}

{"title":"O-GlcNAcylation promotes angiogenic transdifferentiation to reverse vascular ischemia","authors":"Shuang Li, Alexander J. Lu, Eric S. Nagueh, Yanqiang Li, Michael Graber, Kaylee N. Carter, Elisa Morales, Crystina L. Kriss, Kaifu Chen, Junchen Liu, Guangyu Wang, John P. Cooke, Li Lai","doi":"10.1038/s44161-025-00673-7","DOIUrl":"10.1038/s44161-025-00673-7","url":null,"abstract":"The restoration of the microvasculature is essential to cardiovascular regeneration. Our previous work demonstrated that angiogenic transdifferentiation of fibroblasts into endothelial cells facilitates vascular recovery following limb ischemia and is accompanied by a metabolic shift toward glycolysis. However, a comprehensive characterization of the metabolic alterations that contribute to the transdifferentiation process is still lacking. Here we identify a marked upregulation of uridine diphosphate N-acetylglucosamine (UDP-GlcNAc), the substrate for O-GlcNAcylation, during transdifferentiation. Enhancing this pathway promotes, whereas inhibiting it impairs, the efficiency of transdifferentiation. Mechanistically, we demonstrate that O-GlcNAcylation facilitates chromatin remodeling through modification of HIRA, a histone chaperone responsible for de novo deposition of the noncanonical histone variant H3.3, a process intimately linked to transcriptional activation. These findings are further supported by in vivo lineage tracing and conditional knockout mouse models. Collectively, our study demonstrates that O-GlcNAcylation enhances angiogenic transdifferentiation through a metabolic-and-epigenetic-coupled mechanism, thereby strengthening vascular recovery. Li, Lu et al. demonstrate that O-GlcNAcylation enhances angiogenic transdifferentiation from fibroblasts to endothelial cells through a HIRA-dependent H3.3 deposition mechanism and facilitates vascular regeneration.","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"4 7","pages":"904-920"},"PeriodicalIF":10.8,"publicationDate":"2025-07-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144565497","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}

{"title":"Transcriptional changes of the extracellular matrix in chronic thromboembolic pulmonary hypertension govern right ventricle remodeling and recovery","authors":"Leili Jafari, Christoph B. Wiedenroth, Steffen D. Kriechbaum, Dimitri Grün, Prakash Chelladurai, Stefan Guenther, Carsten Kuenne, Alicia M. Späth, Anoop V. Cherian, Christian Troidl, Jochen Wilhelm, Stanislav Keranov, Till Keller, Baktybek Kojonazarov, Ralph T. Schermuly, Stefan Guth, Oliver Dörr, Holger Nef, Mario Boehm, Edda Spiekerkoetter, Przemyslaw Leszek, Zoltan V. Varga, Peter Ferdinandy, Hossein A. Ghofrani, Peter Dorfmüller, Norbert Weißmann, Christian W. Hamm, Eckhard Mayer, Werner Seeger, Christoph Liebetrau, Soni Savai Pullamsetti","doi":"10.1038/s44161-025-00672-8","DOIUrl":"10.1038/s44161-025-00672-8","url":null,"abstract":"Chronic thromboembolic pulmonary hypertension (CTEPH) leads to progressive right ventricular (RV) dysfunction. Pulmonary endarterectomy (PEA) is an established treatment for these patients; however, the molecular mechanisms underlying RV remodeling and recovery remain poorly understood. Here we show that RNA sequencing and histological analysis of RV free wall and septal biopsies from patients with CTEPH reveal extracellular matrix enrichment and cytoskeletal remodeling before PEA. These changes were consistent across an exploratory and confirmatory cohort. Post-PEA samples showed reversal of both histological and transcriptional abnormalities. Key signaling molecules—ANKRD1, IL7R and SERPINE1—were implicated in fibrotic and proliferative pathways, as confirmed in human tissues and experimental models. Our findings identify a reversible gene expression and structural remodeling signature in the RV, linking hemodynamic unloading with molecular recovery. These insights suggest potential therapeutic targets to modulate maladaptive RV remodeling in CTEPH and improve outcomes beyond surgical intervention. Through RNA profiling of right ventricular tissue from patients with chronic thromboembolic pulmonary hypertension, Jafari et al. uncover mechanisms underlying disease severity-associated remodeling, identify key signaling molecules involved in fibrotic and proliferative pathways, and reveal processes driving right ventricular recovery after pulmonary endarterectomy.","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"4 7","pages":"857-875"},"PeriodicalIF":10.8,"publicationDate":"2025-07-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12259468/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144565498","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}

{"title":"Hemolyzed red blood cells prevent microvascular bleeding in ischemic organs","authors":"Gerburg Schwaerzer","doi":"10.1038/s44161-025-00689-z","DOIUrl":"10.1038/s44161-025-00689-z","url":null,"abstract":"","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"4 7","pages":"793-793"},"PeriodicalIF":10.8,"publicationDate":"2025-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144556051","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}

{"title":"Multimodal AI to forecast arrhythmic death in hypertrophic cardiomyopathy","authors":"Changxin Lai, Minglang Yin, Eugene G. Kholmovski, Dan M. Popescu, Dai-Yin Lu, Erica Scherer, Edem Binka, Stefan L. Zimmerman, Jonathan Chrispin, Allison G. Hays, Dermot M. Phelan, M. Roselle Abraham, Natalia A. Trayanova","doi":"10.1038/s44161-025-00679-1","DOIUrl":"10.1038/s44161-025-00679-1","url":null,"abstract":"Sudden cardiac death from ventricular arrhythmias is a leading cause of mortality worldwide. Arrhythmic death prognostication is challenging in patients with hypertrophic cardiomyopathy (HCM), a setting where current clinical guidelines show low performance and inconsistent accuracy. Here, we present a deep learning approach, MAARS (Multimodal Artificial intelligence for ventricular Arrhythmia Risk Stratification), to forecast lethal arrhythmia events in patients with HCM by analyzing multimodal medical data. MAARS’ transformer-based neural networks learn from electronic health records, echocardiogram and radiology reports, and contrast-enhanced cardiac magnetic resonance images, the latter being a unique feature of this model. MAARS achieves an area under the curve of 0.89 (95% confidence interval (CI) 0.79–0.94) and 0.81 (95% CI 0.69–0.93) in internal and external cohorts and outperforms current clinical guidelines by 0.27–0.35 (internal) and 0.22–0.30 (external). In contrast to clinical guidelines, it demonstrates fairness across demographic subgroups. We interpret MAARS’ predictions on multiple levels to promote artificial intelligence transparency and derive risk factors warranting further investigation. Lai et al. present the machine learning model MAARS to predict arrhythmic sudden cardiac death from multimodal imaging and clinical data in patients with hypertrophic cardiomyopathy.","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"4 7","pages":"891-903"},"PeriodicalIF":10.8,"publicationDate":"2025-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12259465/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144556052","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}

{"title":"Milli-spinner promises faster and safer blood clot removal","authors":"Elisa Martini","doi":"10.1038/s44161-025-00690-6","DOIUrl":"10.1038/s44161-025-00690-6","url":null,"abstract":"","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"4 7","pages":"792-792"},"PeriodicalIF":10.8,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144546424","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}