Pub Date : 2025-06-22DOI: 10.1038/s41569-025-01166-7
Mathias Mericskay, Coert J. Zuurbier, Lisa C. Heather, Anja Karlstaedt, Javier Inserte, Luc Bertrand, Georgios Kararigas, Marisol Ruiz-Meana, Christoph Maack, Gabriele G. Schiattarella
The number of patients with heart failure is expected to rise sharply owing to ageing populations, poor dietary habits, unhealthy lifestyles and improved survival rates from conditions such as hypertension and myocardial infarction. Heart failure is classified into two main types: heart failure with reduced ejection fraction (HFrEF) and heart failure with preserved ejection fraction (HFpEF). These forms fundamentally differ, especially in how metabolism is regulated, but they also have shared features such as mitochondrial dysfunction. HFrEF is typically driven by neuroendocrine activation and mechanical strain, which demands a higher ATP production to sustain cardiac contraction. However, the primary energy source in a healthy heart (fatty acid β-oxidation) is often suppressed in HFrEF. Although glucose uptake increases in HFrEF, mitochondrial dysfunction disrupts glucose oxidation, and glycolysis and ketone oxidation only partially compensate for this imbalance. Conversely, HFpEF, particularly in individuals with metabolic diseases, such as obesity or type 2 diabetes mellitus, results from both mechanical and metabolic overload. Elevated glucose and lipid levels overwhelm normal metabolic pathways, leading to an accumulation of harmful metabolic byproducts that impair mitochondrial and cellular function. In this Review, we explore how disruptions in cardiac metabolism are not only markers of heart failure but also key drivers of disease progression. We also examine how metabolic intermediates influence signalling pathways that modify proteins and regulate gene expression in the heart. The growing recognition of the role of metabolic alterations in heart failure has led to groundbreaking treatments that target these metabolic disruptions, offering new hope for these patients. In this Review, Mericskay and colleagues discuss the role of cardiac intermediary metabolism in heart failure, describing the perturbations in cardiac energy metabolism that occur in heart failure with reduced ejection fraction and cardiometabolic heart failure with preserved ejection fraction, and highlighting potential treatments to target intermediary metabolism in these patients.
{"title":"Cardiac intermediary metabolism in heart failure: substrate use, signalling roles and therapeutic targets","authors":"Mathias Mericskay, Coert J. Zuurbier, Lisa C. Heather, Anja Karlstaedt, Javier Inserte, Luc Bertrand, Georgios Kararigas, Marisol Ruiz-Meana, Christoph Maack, Gabriele G. Schiattarella","doi":"10.1038/s41569-025-01166-7","DOIUrl":"10.1038/s41569-025-01166-7","url":null,"abstract":"The number of patients with heart failure is expected to rise sharply owing to ageing populations, poor dietary habits, unhealthy lifestyles and improved survival rates from conditions such as hypertension and myocardial infarction. Heart failure is classified into two main types: heart failure with reduced ejection fraction (HFrEF) and heart failure with preserved ejection fraction (HFpEF). These forms fundamentally differ, especially in how metabolism is regulated, but they also have shared features such as mitochondrial dysfunction. HFrEF is typically driven by neuroendocrine activation and mechanical strain, which demands a higher ATP production to sustain cardiac contraction. However, the primary energy source in a healthy heart (fatty acid β-oxidation) is often suppressed in HFrEF. Although glucose uptake increases in HFrEF, mitochondrial dysfunction disrupts glucose oxidation, and glycolysis and ketone oxidation only partially compensate for this imbalance. Conversely, HFpEF, particularly in individuals with metabolic diseases, such as obesity or type 2 diabetes mellitus, results from both mechanical and metabolic overload. Elevated glucose and lipid levels overwhelm normal metabolic pathways, leading to an accumulation of harmful metabolic byproducts that impair mitochondrial and cellular function. In this Review, we explore how disruptions in cardiac metabolism are not only markers of heart failure but also key drivers of disease progression. We also examine how metabolic intermediates influence signalling pathways that modify proteins and regulate gene expression in the heart. The growing recognition of the role of metabolic alterations in heart failure has led to groundbreaking treatments that target these metabolic disruptions, offering new hope for these patients. In this Review, Mericskay and colleagues discuss the role of cardiac intermediary metabolism in heart failure, describing the perturbations in cardiac energy metabolism that occur in heart failure with reduced ejection fraction and cardiometabolic heart failure with preserved ejection fraction, and highlighting potential treatments to target intermediary metabolism in these patients.","PeriodicalId":18976,"journal":{"name":"Nature Reviews Cardiology","volume":"22 10","pages":"704-727"},"PeriodicalIF":44.2,"publicationDate":"2025-06-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144337472","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-06-22DOI: 10.1038/s41569-025-01181-8
Christoph Maack
Metabolic diseases are important risk factors for the development of heart failure, and energetic deficit and oxidative stress are important in its pathophysiology. A Focus issue in Nature Reviews Cardiology appraises the metabolic alterations in heart failure, with an emphasis on substrate and intermediate metabolism, vascular dysfunction, inflammation and mechano-energetic uncoupling, integrating these different pathomechanistic angles into one cohesive view.
{"title":"Metabolic alterations in heart failure","authors":"Christoph Maack","doi":"10.1038/s41569-025-01181-8","DOIUrl":"10.1038/s41569-025-01181-8","url":null,"abstract":"Metabolic diseases are important risk factors for the development of heart failure, and energetic deficit and oxidative stress are important in its pathophysiology. A Focus issue in Nature Reviews Cardiology appraises the metabolic alterations in heart failure, with an emphasis on substrate and intermediate metabolism, vascular dysfunction, inflammation and mechano-energetic uncoupling, integrating these different pathomechanistic angles into one cohesive view.","PeriodicalId":18976,"journal":{"name":"Nature Reviews Cardiology","volume":"22 10","pages":"695-696"},"PeriodicalIF":44.2,"publicationDate":"2025-06-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144337507","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-06-22DOI: 10.1038/s41569-025-01165-8
Ioanna Andreadou, Alessandra Ghigo, Panagiota-Efstathia Nikolaou, Filip K. Swirski, James T. Thackeray, Gerd Heusch, Gemma Vilahur
The interaction between inflammation and metabolism (immunometabolism) is a crucial factor in the pathophysiology of heart failure, whether the cardiac failure originates from ischaemic injury or systemic metabolic disorders, and whether it is associated with reduced or preserved ejection fraction. Ischaemia, metabolic stress and comorbidity-driven systemic inflammation attract innate and adaptive immune cells to the myocardium and induce their polarization towards pro-inflammatory or anti-inflammatory phenotypes through cell-intrinsic metabolic shifts involving oxidative phosphorylation and anaerobic glycolysis. These infiltrating immune cells modulate cardiac and systemic metabolism. The bidirectional metabolic crosstalk between immune cells and parenchymal and stromal cardiac cells contributes to adverse cardiac remodelling. In turn, ischaemic injury and deregulated metabolism stimulate bone marrow and extramedullary myelopoiesis, which increases immune cell recruitment and perpetuates a non-resolving chronic inflammatory state. Pharmacological interventions targeting metabolism have shown promise for improving outcomes in patients with heart failure, but immunomodulatory approaches face multiple challenges. Understanding the complex metabolic pathways and cell–cell interactions that regulate immunometabolism in heart failure is essential to identify new therapies that shift the balance from maladaptive to cardioprotective immune responses. In this Review, we provide a comprehensive overview of the intricate cellular and molecular mechanisms that govern immunometabolism in heart failure and discuss potential approaches to non-invasively monitor and treat patients with heart failure. In this Review, the authors discuss the cellular and molecular mechanisms of immunometabolism in heart failure and highlight potential approaches for non-invasive monitoring and for the treatment of patients with heart failure.
{"title":"Immunometabolism in heart failure","authors":"Ioanna Andreadou, Alessandra Ghigo, Panagiota-Efstathia Nikolaou, Filip K. Swirski, James T. Thackeray, Gerd Heusch, Gemma Vilahur","doi":"10.1038/s41569-025-01165-8","DOIUrl":"10.1038/s41569-025-01165-8","url":null,"abstract":"The interaction between inflammation and metabolism (immunometabolism) is a crucial factor in the pathophysiology of heart failure, whether the cardiac failure originates from ischaemic injury or systemic metabolic disorders, and whether it is associated with reduced or preserved ejection fraction. Ischaemia, metabolic stress and comorbidity-driven systemic inflammation attract innate and adaptive immune cells to the myocardium and induce their polarization towards pro-inflammatory or anti-inflammatory phenotypes through cell-intrinsic metabolic shifts involving oxidative phosphorylation and anaerobic glycolysis. These infiltrating immune cells modulate cardiac and systemic metabolism. The bidirectional metabolic crosstalk between immune cells and parenchymal and stromal cardiac cells contributes to adverse cardiac remodelling. In turn, ischaemic injury and deregulated metabolism stimulate bone marrow and extramedullary myelopoiesis, which increases immune cell recruitment and perpetuates a non-resolving chronic inflammatory state. Pharmacological interventions targeting metabolism have shown promise for improving outcomes in patients with heart failure, but immunomodulatory approaches face multiple challenges. Understanding the complex metabolic pathways and cell–cell interactions that regulate immunometabolism in heart failure is essential to identify new therapies that shift the balance from maladaptive to cardioprotective immune responses. In this Review, we provide a comprehensive overview of the intricate cellular and molecular mechanisms that govern immunometabolism in heart failure and discuss potential approaches to non-invasively monitor and treat patients with heart failure. In this Review, the authors discuss the cellular and molecular mechanisms of immunometabolism in heart failure and highlight potential approaches for non-invasive monitoring and for the treatment of patients with heart failure.","PeriodicalId":18976,"journal":{"name":"Nature Reviews Cardiology","volume":"22 10","pages":"751-772"},"PeriodicalIF":44.2,"publicationDate":"2025-06-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144337525","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-06-22DOI: 10.1038/s41569-025-01163-w
Luca Liberale, Dirk Jan Duncker, Derek John Hausenloy, Simon Kraler, Hans Erik Bøtker, Bruno Karl Podesser, Gerd Heusch, Petra Kleinbongard
Heart failure (HF) is not confined to contractile failure of cardiomyocytes or myocardial fibrosis. Coronary and systemic vascular dysfunction contributes to the initiation and progression of HF with or without reduced ejection fraction. Furthermore, HF compromises vascular function, creating and sustaining a vicious cycle with deranging effects on coronary blood flow, cardiac metabolism and cardiac function. In HF, systemic arterial dysfunction, characterized by increased arterial stiffness and resistance, raises cardiac afterload and impedes myocardial contractile function. Reduced coronary blood flow impairs myocardial oxygen delivery and consequently cardiomyocyte metabolism and function. Coronary microvascular dysfunction is heterogeneous in its pathogenesis and manifestations, complicating the diagnosis and management across different HF phenotypes. Understanding the alterations in function in different segments of the vasculature, from the aorta to the capillary level, offers mechanistic insights into disease drivers and therapeutic interventions. Interventional approaches can improve vascular haemodynamics, whereas established and emerging pharmacotherapies target the neurohumoral axis and reduce extravascular compression, inflammation, and oxidative stress, thereby improving vascular function and HF-related outcomes. In this Review, we provide a mechanistic framework of vascular dysfunction in the pathogenesis of HF with or without reduced ejection fraction, pointing towards integrated therapies that consider the vascular implications of contemporary HF management across HF phenotypes. Coronary and systemic vascular dysfunction contributes to the initiation and progression of heart failure (HF) with or without reduced ejection fraction and, vice versa, HF compromises vascular function. In this Review, Liberale and colleagues discuss vascular dysfunction in the pathogenesis of HF and how pharmacological, interventional and surgical management of HF can improve vascular function.
{"title":"Vascular (dys)function in the failing heart","authors":"Luca Liberale, Dirk Jan Duncker, Derek John Hausenloy, Simon Kraler, Hans Erik Bøtker, Bruno Karl Podesser, Gerd Heusch, Petra Kleinbongard","doi":"10.1038/s41569-025-01163-w","DOIUrl":"10.1038/s41569-025-01163-w","url":null,"abstract":"Heart failure (HF) is not confined to contractile failure of cardiomyocytes or myocardial fibrosis. Coronary and systemic vascular dysfunction contributes to the initiation and progression of HF with or without reduced ejection fraction. Furthermore, HF compromises vascular function, creating and sustaining a vicious cycle with deranging effects on coronary blood flow, cardiac metabolism and cardiac function. In HF, systemic arterial dysfunction, characterized by increased arterial stiffness and resistance, raises cardiac afterload and impedes myocardial contractile function. Reduced coronary blood flow impairs myocardial oxygen delivery and consequently cardiomyocyte metabolism and function. Coronary microvascular dysfunction is heterogeneous in its pathogenesis and manifestations, complicating the diagnosis and management across different HF phenotypes. Understanding the alterations in function in different segments of the vasculature, from the aorta to the capillary level, offers mechanistic insights into disease drivers and therapeutic interventions. Interventional approaches can improve vascular haemodynamics, whereas established and emerging pharmacotherapies target the neurohumoral axis and reduce extravascular compression, inflammation, and oxidative stress, thereby improving vascular function and HF-related outcomes. In this Review, we provide a mechanistic framework of vascular dysfunction in the pathogenesis of HF with or without reduced ejection fraction, pointing towards integrated therapies that consider the vascular implications of contemporary HF management across HF phenotypes. Coronary and systemic vascular dysfunction contributes to the initiation and progression of heart failure (HF) with or without reduced ejection fraction and, vice versa, HF compromises vascular function. In this Review, Liberale and colleagues discuss vascular dysfunction in the pathogenesis of HF and how pharmacological, interventional and surgical management of HF can improve vascular function.","PeriodicalId":18976,"journal":{"name":"Nature Reviews Cardiology","volume":"22 10","pages":"728-750"},"PeriodicalIF":44.2,"publicationDate":"2025-06-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144337490","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-06-12DOI: 10.1038/s41569-025-01182-7
Karina Huynh
A new study in science Translational Medicine demonstrates that the atheroprotective effects of PPARα agonists are associated with their anti-inflammatory properties rather than their lipid-lowering activity, highlighting the importance of targeting inflammation in managing the residual risk of cardiovascular disease
{"title":"Atheroprotection mediated by hepatic PPARα is linked to its anti-inflammatory, but not lipid-lowering, properties","authors":"Karina Huynh","doi":"10.1038/s41569-025-01182-7","DOIUrl":"10.1038/s41569-025-01182-7","url":null,"abstract":"A new study in science Translational Medicine demonstrates that the atheroprotective effects of PPARα agonists are associated with their anti-inflammatory properties rather than their lipid-lowering activity, highlighting the importance of targeting inflammation in managing the residual risk of cardiovascular disease","PeriodicalId":18976,"journal":{"name":"Nature Reviews Cardiology","volume":"22 8","pages":"533-533"},"PeriodicalIF":44.2,"publicationDate":"2025-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144268539","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-06-06DOI: 10.1038/s41569-025-01178-3
Steven Niederer, Henry Chubb, Kenneth C. Bilchick, Christopher Aldo Rinaldi
Cardiac resynchronization therapy is used to treat dyssynchronous heart failure. Lead-related complications and anatomical constraints can limit pacing lead placement, but leadless systems are now becoming available. These new systems overcome lead-related issues, offering a new option for patients with complex disease (such as congenital heart disease) by eliminating intravascular hardware.
{"title":"Leadless and extravascular cardiac resynchronization therapy: the future for CRT?","authors":"Steven Niederer, Henry Chubb, Kenneth C. Bilchick, Christopher Aldo Rinaldi","doi":"10.1038/s41569-025-01178-3","DOIUrl":"10.1038/s41569-025-01178-3","url":null,"abstract":"Cardiac resynchronization therapy is used to treat dyssynchronous heart failure. Lead-related complications and anatomical constraints can limit pacing lead placement, but leadless systems are now becoming available. These new systems overcome lead-related issues, offering a new option for patients with complex disease (such as congenital heart disease) by eliminating intravascular hardware.","PeriodicalId":18976,"journal":{"name":"Nature Reviews Cardiology","volume":"22 8","pages":"529-531"},"PeriodicalIF":44.2,"publicationDate":"2025-06-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144237229","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-06-05DOI: 10.1038/s41569-025-01171-w
Tomàs Pinós, Richard M. Cubbon, Alfredo Santalla, Carmen Fiuza-Luces, Alejandro Santos-Lozano, Miguel A. Martín, Joaquín Arenas, Joachim Nielsen, Niels Ørtenblad, Alejandro Lucia
Glycogen storage diseases are rare conditions affecting both sexes that are caused by inherited deficiencies of enzymes involved either in glycogen synthesis or breakdown, or in glycolysis. The liver and skeletal muscle are usually the most affected tissues. However, because glycogen has an important role in cardiac development and function, several glycogen storage diseases are associated, at least indirectly, with cardiac disorders, some of which have severe consequences from the first months of life. Early identification of these conditions is, therefore, an important issue, and implementation of strategies to prevent fatal outcomes due to cardiovascular disease is vital. In this Review, we discuss the pathophysiological mechanisms and the preclinical, clinical and epidemiological evidence for cardiovascular involvement in various glycogen storage diseases. We also describe interventions that can help preserve heart function, including changes in nutrition and exercise, as well as the few available molecular therapies to address the underlying metabolic anomalies. Glycogen has an important role in cardiac development and function. In this Review, Pinós and colleagues discuss the cardiovascular manifestations of glycogen storage diseases caused by rare inherited deficiencies of enzymes involved either in glycogen synthesis or breakdown, or in glycolysis. Interventions, including gene therapies, for these conditions are also summarized.
{"title":"Cardiovascular involvement in glycogen storage diseases","authors":"Tomàs Pinós, Richard M. Cubbon, Alfredo Santalla, Carmen Fiuza-Luces, Alejandro Santos-Lozano, Miguel A. Martín, Joaquín Arenas, Joachim Nielsen, Niels Ørtenblad, Alejandro Lucia","doi":"10.1038/s41569-025-01171-w","DOIUrl":"10.1038/s41569-025-01171-w","url":null,"abstract":"Glycogen storage diseases are rare conditions affecting both sexes that are caused by inherited deficiencies of enzymes involved either in glycogen synthesis or breakdown, or in glycolysis. The liver and skeletal muscle are usually the most affected tissues. However, because glycogen has an important role in cardiac development and function, several glycogen storage diseases are associated, at least indirectly, with cardiac disorders, some of which have severe consequences from the first months of life. Early identification of these conditions is, therefore, an important issue, and implementation of strategies to prevent fatal outcomes due to cardiovascular disease is vital. In this Review, we discuss the pathophysiological mechanisms and the preclinical, clinical and epidemiological evidence for cardiovascular involvement in various glycogen storage diseases. We also describe interventions that can help preserve heart function, including changes in nutrition and exercise, as well as the few available molecular therapies to address the underlying metabolic anomalies. Glycogen has an important role in cardiac development and function. In this Review, Pinós and colleagues discuss the cardiovascular manifestations of glycogen storage diseases caused by rare inherited deficiencies of enzymes involved either in glycogen synthesis or breakdown, or in glycolysis. Interventions, including gene therapies, for these conditions are also summarized.","PeriodicalId":18976,"journal":{"name":"Nature Reviews Cardiology","volume":"23 1","pages":"39-59"},"PeriodicalIF":44.2,"publicationDate":"2025-06-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144218799","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-06-03DOI: 10.1038/s41569-025-01177-4
Gareth Owens
Aortic dissection has long been considered a rare, unpreventable and inevitably fatal disease. However, recent advances now prove otherwise. The patient-led Think Aorta campaign is challenging old thinking, improving diagnosis and advocating for better care, such as family screening. Patient advocacy and recent international guidelines classifying the aorta as an organ are catalysts for further improvements in patient care.
{"title":"Think Aorta: aortic dissection awareness and perspectives from the patient","authors":"Gareth Owens","doi":"10.1038/s41569-025-01177-4","DOIUrl":"10.1038/s41569-025-01177-4","url":null,"abstract":"Aortic dissection has long been considered a rare, unpreventable and inevitably fatal disease. However, recent advances now prove otherwise. The patient-led Think Aorta campaign is challenging old thinking, improving diagnosis and advocating for better care, such as family screening. Patient advocacy and recent international guidelines classifying the aorta as an organ are catalysts for further improvements in patient care.","PeriodicalId":18976,"journal":{"name":"Nature Reviews Cardiology","volume":"22 8","pages":"527-528"},"PeriodicalIF":44.2,"publicationDate":"2025-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144201638","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-05-29DOI: 10.1038/s41569-025-01174-7
Purvi Parwani, F. Aaysha Cader
Effective engagement with cardiovascular societies enhances professional development, academic growth and leadership opportunities. We describe practical strategies for cardiovascular professionals to connect with their peers, seek mentorship, advance professionally and contribute as active members of the cardiovascular society, to develop an impactful career and advance the field of cardiac medicine.
{"title":"Networking effectively with cardiovascular societies: strategies for meaningful engagement and career advancement","authors":"Purvi Parwani, F. Aaysha Cader","doi":"10.1038/s41569-025-01174-7","DOIUrl":"10.1038/s41569-025-01174-7","url":null,"abstract":"Effective engagement with cardiovascular societies enhances professional development, academic growth and leadership opportunities. We describe practical strategies for cardiovascular professionals to connect with their peers, seek mentorship, advance professionally and contribute as active members of the cardiovascular society, to develop an impactful career and advance the field of cardiac medicine.","PeriodicalId":18976,"journal":{"name":"Nature Reviews Cardiology","volume":"22 7","pages":"461-462"},"PeriodicalIF":44.2,"publicationDate":"2025-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144164849","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-05-28DOI: 10.1038/s41569-025-01176-5
Sepiso K. Masenga, Annet Kirabo
{"title":"Reply to ‘Neuroendocrine regulatory effects of sex hormones on salt sensitivity of blood pressure’","authors":"Sepiso K. Masenga, Annet Kirabo","doi":"10.1038/s41569-025-01176-5","DOIUrl":"10.1038/s41569-025-01176-5","url":null,"abstract":"","PeriodicalId":18976,"journal":{"name":"Nature Reviews Cardiology","volume":"22 9","pages":"690-691"},"PeriodicalIF":44.2,"publicationDate":"2025-05-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144153483","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
京公网安备 11010802042870号
京ICP备2023020795号-1
扫码关注我们
求助内容：
应助结果提醒方式：