Pub Date : 2026-01-02DOI: 10.1038/s44161-025-00764-5
Elisa Martini
{"title":"Loss of function of the obesity-associated gene MC4R reduces cardiovascular risk and increases lipid clearance","authors":"Elisa Martini","doi":"10.1038/s44161-025-00764-5","DOIUrl":"10.1038/s44161-025-00764-5","url":null,"abstract":"","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"5 1","pages":"4-4"},"PeriodicalIF":10.8,"publicationDate":"2026-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145893547","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}
Pub Date : 2025-12-29DOI: 10.1038/s44161-025-00755-6
Irfan S. Kathiriya, Martin H. Dominguez, Kavitha S. Rao, Jonathon M. Muncie-Vasic, W. Patrick Devine, Kevin M. Hu, Swetansu K. Hota, Bayardo I. Garay, Diego Quintero, Piyush Goyal, Megan N. Matthews, Reuben Thomas, Tatyana Sukonnik, Dario Miguel-Perez, Sarah Winchester, Emily F. Brower, André Forjaz, Pei-Hsun Wu, Denis Wirtz, Ashley L. Kiemen, Benoit G. Bruneau
Failure of septation of the interventricular septum (IVS) is the most common congenital heart defect, but mechanisms for patterning the IVS are largely unknown. Here we show that a Tbx5+/Mef2cAHF+ progenitor lineage forms a compartment boundary bisecting the IVS. This coordinated population originates at a first and second heart field interface. Ablation of Tbx5+/Mef2cAHF+ progenitors causes IVS disorganization, right ventricular hypoplasia and mixing of IVS lineages. Reduced dosage of the congenital heart defect transcription factor TBX5 disrupts boundary position and integrity, resulting in ventricular septation defects and patterning defects, including misexpression of Slit2 and Ntn1, which encode guidance cues. Reducing NTN1 dosage partly rescues cardiac defects in Tbx5 mutant embryos. Loss of Slit2 or Ntn1 causes ventricular septation defects and perturbed septal lineage distributions. Thus, we identify Tbx5 as a candidate selector gene, directing progenitors and regulating essential cues, to pattern a compartment boundary for proper cardiac septation, revealing mechanisms for cardiac birth defects. Kathiriya et al. identify a cardiac progenitor lineage with expression of Tbx5 and anterior heart field-specific expression of Mef2c that bisects the intraventricular septum during development and show that alterations in this lineage lead to congenital heart defects in mice.
{"title":"A disrupted compartment boundary underlies abnormal cardiac patterning and congenital heart defects","authors":"Irfan S. Kathiriya, Martin H. Dominguez, Kavitha S. Rao, Jonathon M. Muncie-Vasic, W. Patrick Devine, Kevin M. Hu, Swetansu K. Hota, Bayardo I. Garay, Diego Quintero, Piyush Goyal, Megan N. Matthews, Reuben Thomas, Tatyana Sukonnik, Dario Miguel-Perez, Sarah Winchester, Emily F. Brower, André Forjaz, Pei-Hsun Wu, Denis Wirtz, Ashley L. Kiemen, Benoit G. Bruneau","doi":"10.1038/s44161-025-00755-6","DOIUrl":"10.1038/s44161-025-00755-6","url":null,"abstract":"Failure of septation of the interventricular septum (IVS) is the most common congenital heart defect, but mechanisms for patterning the IVS are largely unknown. Here we show that a Tbx5+/Mef2cAHF+ progenitor lineage forms a compartment boundary bisecting the IVS. This coordinated population originates at a first and second heart field interface. Ablation of Tbx5+/Mef2cAHF+ progenitors causes IVS disorganization, right ventricular hypoplasia and mixing of IVS lineages. Reduced dosage of the congenital heart defect transcription factor TBX5 disrupts boundary position and integrity, resulting in ventricular septation defects and patterning defects, including misexpression of Slit2 and Ntn1, which encode guidance cues. Reducing NTN1 dosage partly rescues cardiac defects in Tbx5 mutant embryos. Loss of Slit2 or Ntn1 causes ventricular septation defects and perturbed septal lineage distributions. Thus, we identify Tbx5 as a candidate selector gene, directing progenitors and regulating essential cues, to pattern a compartment boundary for proper cardiac septation, revealing mechanisms for cardiac birth defects. Kathiriya et al. identify a cardiac progenitor lineage with expression of Tbx5 and anterior heart field-specific expression of Mef2c that bisects the intraventricular septum during development and show that alterations in this lineage lead to congenital heart defects in mice.","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"5 1","pages":"67-83"},"PeriodicalIF":10.8,"publicationDate":"2025-12-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s44161-025-00755-6.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145859468","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}
Pub Date : 2025-12-29DOI: 10.1038/s44161-025-00757-4
Khaled Rjoob, Kathryn A. McGurk, Sean L. Zheng, Lara Curran, Mahmoud Ibrahim, Lingyao Zeng, Vladislav Kim, Shamin Tahasildar, Soodeh Kalaie, Deva S. Senevirathne, Parisa Gifani, Vladimir Losev, Jin Zheng, Wenjia Bai, Antonio de Marvao, James S. Ware, Christian Bender, Declan P. O’Regan
Understanding gene–disease associations is important for uncovering pathological mechanisms and identifying potential therapeutic targets. Knowledge graphs can represent and integrate data from multiple biomedical sources, but lack individual-level information on target organ structure and function. Here we develop CardioKG, a knowledge graph that integrates over 200,000 computer vision-derived cardiovascular phenotypes from biomedical images with data extracted from 18 biological databases to model over a million relationships. We used a variational graph auto-encoder to generate node embeddings from the knowledge graph to predict gene–disease associations, assess druggability and identify drug repurposing strategies. The model predicted genetic associations and therapeutic opportunities for leading causes of cardiovascular disease, which were associated with improved survival. Candidate therapies included methotrexate for heart failure and gliptins for atrial fibrillation, and the addition of imaging data enhanced pathway discovery. These capabilities support the use of biomedical imaging to enhance graph-structured models for identifying treatable disease mechanisms. Rjoob et al. develop CardioKG, a knowledge graph built on cardiac imaging traits to identify genetic associations and potential therapeutic strategies and drug repurposing opportunities for cardiovascular diseases.
{"title":"A multimodal vision knowledge graph of cardiovascular disease","authors":"Khaled Rjoob, Kathryn A. McGurk, Sean L. Zheng, Lara Curran, Mahmoud Ibrahim, Lingyao Zeng, Vladislav Kim, Shamin Tahasildar, Soodeh Kalaie, Deva S. Senevirathne, Parisa Gifani, Vladimir Losev, Jin Zheng, Wenjia Bai, Antonio de Marvao, James S. Ware, Christian Bender, Declan P. O’Regan","doi":"10.1038/s44161-025-00757-4","DOIUrl":"10.1038/s44161-025-00757-4","url":null,"abstract":"Understanding gene–disease associations is important for uncovering pathological mechanisms and identifying potential therapeutic targets. Knowledge graphs can represent and integrate data from multiple biomedical sources, but lack individual-level information on target organ structure and function. Here we develop CardioKG, a knowledge graph that integrates over 200,000 computer vision-derived cardiovascular phenotypes from biomedical images with data extracted from 18 biological databases to model over a million relationships. We used a variational graph auto-encoder to generate node embeddings from the knowledge graph to predict gene–disease associations, assess druggability and identify drug repurposing strategies. The model predicted genetic associations and therapeutic opportunities for leading causes of cardiovascular disease, which were associated with improved survival. Candidate therapies included methotrexate for heart failure and gliptins for atrial fibrillation, and the addition of imaging data enhanced pathway discovery. These capabilities support the use of biomedical imaging to enhance graph-structured models for identifying treatable disease mechanisms. Rjoob et al. develop CardioKG, a knowledge graph built on cardiac imaging traits to identify genetic associations and potential therapeutic strategies and drug repurposing opportunities for cardiovascular diseases.","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"5 1","pages":"18-33"},"PeriodicalIF":10.8,"publicationDate":"2025-12-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s44161-025-00757-4.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145859527","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}
Pub Date : 2025-12-17DOI: 10.1038/s44161-025-00765-4
Ziad Mallat
The 2025 Nobel Prize in Physiology or Medicine honored a scientific breakthrough with hidden cardiovascular potential: regulatory T cells and peripheral immune tolerance. These mechanisms provide a paradigm shift for understanding and treating cardiovascular disease, dampening inflammation without compromising immunity, and offering safer and more effective therapies.
{"title":"Translating Nobel Prize-winning Treg cell science into cardiovascular therapy","authors":"Ziad Mallat","doi":"10.1038/s44161-025-00765-4","DOIUrl":"10.1038/s44161-025-00765-4","url":null,"abstract":"The 2025 Nobel Prize in Physiology or Medicine honored a scientific breakthrough with hidden cardiovascular potential: regulatory T cells and peripheral immune tolerance. These mechanisms provide a paradigm shift for understanding and treating cardiovascular disease, dampening inflammation without compromising immunity, and offering safer and more effective therapies.","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"5 1","pages":"1-3"},"PeriodicalIF":10.8,"publicationDate":"2025-12-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145776525","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}
Pub Date : 2025-12-16DOI: 10.1038/s44161-025-00749-4
Art Schuermans, Andreas Verstraete, Vilma Lammi, Tomoko Nakanishi, Maddalena Ardissino, Jef Van den Eynde, Benjamin B. Sun, Marios K. Georgakis, Beatriz Guillen-Guio, Louise V. Wain, Christopher E. Brightling, PHOSP-COVID Collaborative Group, Johan Van Weyenbergh, Adam J. Lewandowski, Betty Raman, Hugo Zeberg, Hanna M. Ollila, Stephen Burgess, Pradeep Natarajan, Michael C. Honigberg, Kathleen Freson, Thomas Vanassche, Peter Verhamme
SARS-CoV-2 infection can result in long COVID, characterized by post-acute symptoms from multiple organs. Current hypotheses on mechanisms underlying long COVID include persistent inflammation and thromboembolism; however, compelling evidence from humans is limited and causal associations remain unclear. In this study, we tested the association of thromboembolism-related genetic variants with long COVID in the Long COVID Host Genetics Initiative (ncases = 3,018; ncontrols = 994,582). Primary analyses revealed that each unit increase in the log odds of genetically predicted venous thromboembolism risk was associated with 1.21-fold odds of long COVID (95% confidence interval (CI): 1.08−1.35; P = 1.2 × 10−3). This association was independent of acute COVID-19 severity, was robust across various sensitivity analyses and was replicated in external datasets. Downstream analyses using gene-specific instruments, along with protein and gene expression data, suggested the protease-activated receptor 1 (PAR-1) as a potential molecular contributor to long COVID. These findings provide human genetic evidence implicating shared pathogenetic pathways in thromboembolism and long COVID. Schuermans et al. discovered that genetic predisposition to thromboembolism is associated with a greater risk of post-acute sequelae after SARS-CoV-2 infection, including long COVID, and downstream analyses implicated PAR-1 as a potential contributor to long COVID.
{"title":"Human genetics implicate thromboembolism in the pathogenesis of long COVID in individuals of European ancestry","authors":"Art Schuermans, Andreas Verstraete, Vilma Lammi, Tomoko Nakanishi, Maddalena Ardissino, Jef Van den Eynde, Benjamin B. Sun, Marios K. Georgakis, Beatriz Guillen-Guio, Louise V. Wain, Christopher E. Brightling, PHOSP-COVID Collaborative Group, Johan Van Weyenbergh, Adam J. Lewandowski, Betty Raman, Hugo Zeberg, Hanna M. Ollila, Stephen Burgess, Pradeep Natarajan, Michael C. Honigberg, Kathleen Freson, Thomas Vanassche, Peter Verhamme","doi":"10.1038/s44161-025-00749-4","DOIUrl":"10.1038/s44161-025-00749-4","url":null,"abstract":"SARS-CoV-2 infection can result in long COVID, characterized by post-acute symptoms from multiple organs. Current hypotheses on mechanisms underlying long COVID include persistent inflammation and thromboembolism; however, compelling evidence from humans is limited and causal associations remain unclear. In this study, we tested the association of thromboembolism-related genetic variants with long COVID in the Long COVID Host Genetics Initiative (ncases = 3,018; ncontrols = 994,582). Primary analyses revealed that each unit increase in the log odds of genetically predicted venous thromboembolism risk was associated with 1.21-fold odds of long COVID (95% confidence interval (CI): 1.08−1.35; P = 1.2 × 10−3). This association was independent of acute COVID-19 severity, was robust across various sensitivity analyses and was replicated in external datasets. Downstream analyses using gene-specific instruments, along with protein and gene expression data, suggested the protease-activated receptor 1 (PAR-1) as a potential molecular contributor to long COVID. These findings provide human genetic evidence implicating shared pathogenetic pathways in thromboembolism and long COVID. Schuermans et al. discovered that genetic predisposition to thromboembolism is associated with a greater risk of post-acute sequelae after SARS-CoV-2 infection, including long COVID, and downstream analyses implicated PAR-1 as a potential contributor to long COVID.","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"4 12","pages":"1662-1676"},"PeriodicalIF":10.8,"publicationDate":"2025-12-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145761500","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}
Pub Date : 2025-12-16DOI: 10.1038/s44161-025-00756-5
Frederik Denorme, Robert A. Campbell
Long COVID is a major global health challenge but the underlying mechanisms are unclear, hampering the development of effective therapies. Evidence points to a causal link between thromboembolic processes and symptom persistence, suggesting a role for vascular and coagulation abnormalities in the pathogenesis of this complex syndrome.
{"title":"Linking thromboembolism to the pathogenesis of long COVID","authors":"Frederik Denorme, Robert A. Campbell","doi":"10.1038/s44161-025-00756-5","DOIUrl":"10.1038/s44161-025-00756-5","url":null,"abstract":"Long COVID is a major global health challenge but the underlying mechanisms are unclear, hampering the development of effective therapies. Evidence points to a causal link between thromboembolic processes and symptom persistence, suggesting a role for vascular and coagulation abnormalities in the pathogenesis of this complex syndrome.","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"4 12","pages":"1594-1595"},"PeriodicalIF":10.8,"publicationDate":"2025-12-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145761501","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}
Pub Date : 2025-12-11DOI: 10.1038/s44161-025-00752-9
Abigail V. Giles, Raul Covian, Hiran A. Prag, Nils Burger, Bertrand Lucotte, Chak Shun Yu, Junhui Sun, Elizabeth Murphy, Thomas Krieg, Michael P. Murphy, Robert S. Balaban
The mitochondrial membrane potential (ΔΨm) drives oxidative phosphorylation and alterations contribute to cardiac pathologies, but real-time assessment of ΔΨm has not been possible. Here we describe noninvasive measurements using mitochondrial heme bL and bH absorbances, which rapidly respond to ΔΨm. Multi-wavelength absorbance spectroscopy enabled their continuous monitoring in isolated mitochondria and the perfused heart. Calibration of heme b absorbance in isolated mitochondria revealed that reduced heme bL relative to total reduced heme b (fbL = bL/(bL + bH)) exhibits a sigmoidal relationship with ΔΨm. Extrapolating this relationship to the heart enabled estimation of ΔΨm as 166 ± 18 mV (n = 25, mean ± s.d.). We used this approach to assess how ΔΨm changes during ischemia–reperfusion injury, an unknown limiting the understanding of ischemia–reperfusion injury. In perfused hearts, ΔΨm declined during ischemia and rapidly reestablished upon reperfusion, supported by oxidation of the succinate accumulated during ischemia. These findings expand our understanding of ischemia–reperfusion injury. Giles et al. developed a method for noninvasive absorbance measurement of mitochondrial hemes to monitor the mitochondrial membrane potential in the perfused heart. They then applied this approach to show how the mitochondrial membrane potential changed during cardiac ischemia.
{"title":"Rapid mitochondrial repolarization upon reperfusion after cardiac ischemia","authors":"Abigail V. Giles, Raul Covian, Hiran A. Prag, Nils Burger, Bertrand Lucotte, Chak Shun Yu, Junhui Sun, Elizabeth Murphy, Thomas Krieg, Michael P. Murphy, Robert S. Balaban","doi":"10.1038/s44161-025-00752-9","DOIUrl":"10.1038/s44161-025-00752-9","url":null,"abstract":"The mitochondrial membrane potential (ΔΨm) drives oxidative phosphorylation and alterations contribute to cardiac pathologies, but real-time assessment of ΔΨm has not been possible. Here we describe noninvasive measurements using mitochondrial heme bL and bH absorbances, which rapidly respond to ΔΨm. Multi-wavelength absorbance spectroscopy enabled their continuous monitoring in isolated mitochondria and the perfused heart. Calibration of heme b absorbance in isolated mitochondria revealed that reduced heme bL relative to total reduced heme b (fbL = bL/(bL + bH)) exhibits a sigmoidal relationship with ΔΨm. Extrapolating this relationship to the heart enabled estimation of ΔΨm as 166 ± 18 mV (n = 25, mean ± s.d.). We used this approach to assess how ΔΨm changes during ischemia–reperfusion injury, an unknown limiting the understanding of ischemia–reperfusion injury. In perfused hearts, ΔΨm declined during ischemia and rapidly reestablished upon reperfusion, supported by oxidation of the succinate accumulated during ischemia. These findings expand our understanding of ischemia–reperfusion injury. Giles et al. developed a method for noninvasive absorbance measurement of mitochondrial hemes to monitor the mitochondrial membrane potential in the perfused heart. They then applied this approach to show how the mitochondrial membrane potential changed during cardiac ischemia.","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"4 12","pages":"1627-1641"},"PeriodicalIF":10.8,"publicationDate":"2025-12-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s44161-025-00752-9.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145746016","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}
Autonomic innervation is important for heart development and function, as well as for the response to injury and hemodynamic stress. However, the mechanisms underlying neurocardiac interactions are difficult to investigate in vivo, prompting the need for advanced engineering of in vitro models of innervated cardiac tissues. Here, we review the embryonic development of the heart and postganglionic autonomic neurons and discuss the functional consequences of cardiac autonomic innervation, focusing on its trophic roles in neonatal and adult hearts. We highlight methods for generating functional cardiomyocytes and autonomic neurons from human pluripotent stem cells and discuss the benefits and limitations of existing in vivo and in vitro cardiac innervation models. Lastly, we present a roadmap for the development of high-fidelity, mature pluripotent stem cell-derived models of cardiac autonomic innervation to address outstanding questions in the field. Patsy et al. review the relationship between the heart and the nervous system during development and the functional consequences of cardiac innervation. They describe the generation of cardiomyocytes and autonomic neurons and propose a roadmap toward the development of cardiac innervation models.
{"title":"Development and modeling of cardiac autonomic innervation","authors":"Marisa Patsy, Kyle Ge, Alastair Khodabukus, Nenad Bursac","doi":"10.1038/s44161-025-00746-7","DOIUrl":"10.1038/s44161-025-00746-7","url":null,"abstract":"Autonomic innervation is important for heart development and function, as well as for the response to injury and hemodynamic stress. However, the mechanisms underlying neurocardiac interactions are difficult to investigate in vivo, prompting the need for advanced engineering of in vitro models of innervated cardiac tissues. Here, we review the embryonic development of the heart and postganglionic autonomic neurons and discuss the functional consequences of cardiac autonomic innervation, focusing on its trophic roles in neonatal and adult hearts. We highlight methods for generating functional cardiomyocytes and autonomic neurons from human pluripotent stem cells and discuss the benefits and limitations of existing in vivo and in vitro cardiac innervation models. Lastly, we present a roadmap for the development of high-fidelity, mature pluripotent stem cell-derived models of cardiac autonomic innervation to address outstanding questions in the field. Patsy et al. review the relationship between the heart and the nervous system during development and the functional consequences of cardiac innervation. They describe the generation of cardiomyocytes and autonomic neurons and propose a roadmap toward the development of cardiac innervation models.","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"4 12","pages":"1598-1615"},"PeriodicalIF":10.8,"publicationDate":"2025-12-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145688816","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}
Pub Date : 2025-11-28DOI: 10.1038/s44161-025-00754-7
David A. Kass
There is great interest in modeling human HFpEF in animals to identify underlying mechanisms and ultimately improve sorely needed therapies. Our current models are a step forward but still fall short in several crucial ways, particularly by not capturing the severity of heart failure features common in patients.
{"title":"Modeling HFpEF in animals","authors":"David A. Kass","doi":"10.1038/s44161-025-00754-7","DOIUrl":"10.1038/s44161-025-00754-7","url":null,"abstract":"There is great interest in modeling human HFpEF in animals to identify underlying mechanisms and ultimately improve sorely needed therapies. Our current models are a step forward but still fall short in several crucial ways, particularly by not capturing the severity of heart failure features common in patients.","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"4 12","pages":"1589-1591"},"PeriodicalIF":10.8,"publicationDate":"2025-11-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145643717","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}
Pub Date : 2025-11-25DOI: 10.1038/s44161-025-00759-2
Gerburg Schwaerzer
{"title":"A cardiotropic viral vector can safely and effectively facilitate therapeutic gene delivery to the heart","authors":"Gerburg Schwaerzer","doi":"10.1038/s44161-025-00759-2","DOIUrl":"10.1038/s44161-025-00759-2","url":null,"abstract":"","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"4 12","pages":"1592-1592"},"PeriodicalIF":10.8,"publicationDate":"2025-11-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145607863","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}
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