Pub Date : 2025-05-28DOI: 10.1038/s41569-025-01175-6
Mi Zhou (, ), Bing-hua Wang (, ), Yu-chan Wang (, ), Wen-jun Zhang (, ), Li-xue Yin (, )
{"title":"Neuroendocrine regulatory effects of sex hormones on salt sensitivity of blood pressure","authors":"Mi Zhou \u0000 (, ), Bing-hua Wang \u0000 (, ), Yu-chan Wang \u0000 (, ), Wen-jun Zhang \u0000 (, ), Li-xue Yin \u0000 (, )","doi":"10.1038/s41569-025-01175-6","DOIUrl":"10.1038/s41569-025-01175-6","url":null,"abstract":"","PeriodicalId":18976,"journal":{"name":"Nature Reviews Cardiology","volume":"22 9","pages":"689-689"},"PeriodicalIF":44.2,"publicationDate":"2025-05-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144153577","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 : 2025-05-23DOI: 10.1038/s41569-025-01168-5
Sahej Bains, John R. Giudicessi, Katja E. Odening, Michael J. Ackerman
Cardiovascular diseases are the leading cause of death globally, with cardiac arrhythmias contributing substantially to this burden. Gene therapy, which directly targets the underlying disease pathobiology, offers an appealing treatment strategy for cardiac arrhythmias owing to its potential as a one-time, curative solution. Over the past two decades, substantial efforts have been made to develop new gene therapy approaches that overcome the limitations of conventional treatments. In this Review, we describe the rationale for gene therapy to treat cardiac arrhythmias; discuss advantages and disadvantages of gene silencing, gene replacement, gene suppression-and-replacement and gene editing technologies; summarize vector modalities and delivery approaches used in the field; present examples of gene therapy strategies used for atrial and ventricular arrhythmias; and highlight the current challenges and limitations in the gene therapy field. In this Review, Ackerman and colleagues describe the rationale for gene therapy to treat cardiac arrhythmias; discuss advantages and disadvantages of gene silencing, replacement and editing technologies; summarize vector modalities and delivery approaches; present examples of gene therapy strategies used for atrial and ventricular arrhythmias; and highlight the current challenges and limitations in the gene therapy field.
{"title":"Gene therapy for cardiac arrhythmias","authors":"Sahej Bains, John R. Giudicessi, Katja E. Odening, Michael J. Ackerman","doi":"10.1038/s41569-025-01168-5","DOIUrl":"10.1038/s41569-025-01168-5","url":null,"abstract":"Cardiovascular diseases are the leading cause of death globally, with cardiac arrhythmias contributing substantially to this burden. Gene therapy, which directly targets the underlying disease pathobiology, offers an appealing treatment strategy for cardiac arrhythmias owing to its potential as a one-time, curative solution. Over the past two decades, substantial efforts have been made to develop new gene therapy approaches that overcome the limitations of conventional treatments. In this Review, we describe the rationale for gene therapy to treat cardiac arrhythmias; discuss advantages and disadvantages of gene silencing, gene replacement, gene suppression-and-replacement and gene editing technologies; summarize vector modalities and delivery approaches used in the field; present examples of gene therapy strategies used for atrial and ventricular arrhythmias; and highlight the current challenges and limitations in the gene therapy field. In this Review, Ackerman and colleagues describe the rationale for gene therapy to treat cardiac arrhythmias; discuss advantages and disadvantages of gene silencing, replacement and editing technologies; summarize vector modalities and delivery approaches; present examples of gene therapy strategies used for atrial and ventricular arrhythmias; and highlight the current challenges and limitations in the gene therapy field.","PeriodicalId":18976,"journal":{"name":"Nature Reviews Cardiology","volume":"23 1","pages":"23-38"},"PeriodicalIF":44.2,"publicationDate":"2025-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144130677","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 : 2025-05-22DOI: 10.1038/s41569-025-01173-8
Gregory B. Lim
In the TANDEM and BROADWAY clinical trials, treatment with the CETP inhibitor obicetrapib in addition to background lipid-lowering therapy significantly reduced plasma LDL-cholesterol levels.
{"title":"LDL-cholesterol lowering with obicetrapib","authors":"Gregory B. Lim","doi":"10.1038/s41569-025-01173-8","DOIUrl":"10.1038/s41569-025-01173-8","url":null,"abstract":"In the TANDEM and BROADWAY clinical trials, treatment with the CETP inhibitor obicetrapib in addition to background lipid-lowering therapy significantly reduced plasma LDL-cholesterol levels.","PeriodicalId":18976,"journal":{"name":"Nature Reviews Cardiology","volume":"22 7","pages":"463-463"},"PeriodicalIF":44.2,"publicationDate":"2025-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144113340","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 : 2025-05-20DOI: 10.1038/s41569-025-01170-x
Marta Catarina Almeida, Ricardo Fontes-Carvalho
Conference presentation skills are a crucial, yet often overlooked, element in the dissemination of cardiovascular research. In an era of information overload and digital communication, the ability to clearly and engagingly present scientific data is essential, to ensure that the findings are understood, shared and implemented into clinical practice.
{"title":"From data to impact: why conference presentation skills are essential for cardiovascular research dissemination","authors":"Marta Catarina Almeida, Ricardo Fontes-Carvalho","doi":"10.1038/s41569-025-01170-x","DOIUrl":"10.1038/s41569-025-01170-x","url":null,"abstract":"Conference presentation skills are a crucial, yet often overlooked, element in the dissemination of cardiovascular research. In an era of information overload and digital communication, the ability to clearly and engagingly present scientific data is essential, to ensure that the findings are understood, shared and implemented into clinical practice.","PeriodicalId":18976,"journal":{"name":"Nature Reviews Cardiology","volume":"22 7","pages":"459-460"},"PeriodicalIF":44.2,"publicationDate":"2025-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144096868","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 : 2025-05-19DOI: 10.1038/s41569-025-01172-9
Irene Fernández-Ruiz
Inhibition of mechanotransduction selectively in cardiac fibrolasts, especially when combined with inhibition of transforming growth factor-β signalling, triggers a reversal of fibroblast activation and suppresses fibrosis in diseased hearts.
{"title":"Dual mechanotherapy for the treatment of cardiac fibrosis","authors":"Irene Fernández-Ruiz","doi":"10.1038/s41569-025-01172-9","DOIUrl":"10.1038/s41569-025-01172-9","url":null,"abstract":"Inhibition of mechanotransduction selectively in cardiac fibrolasts, especially when combined with inhibition of transforming growth factor-β signalling, triggers a reversal of fibroblast activation and suppresses fibrosis in diseased hearts.","PeriodicalId":18976,"journal":{"name":"Nature Reviews Cardiology","volume":"22 7","pages":"465-465"},"PeriodicalIF":44.2,"publicationDate":"2025-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144096869","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 : 2025-05-12DOI: 10.1038/s41569-025-01169-4
Karina Huynh
A new study published in Nature reveals the role of the interaction between the circadian transcription factor BMAL1 and hypoxia-inducible factor 2α in circadian-dependent cardioprotection after ischaemia–reperfusion injury, and highlights the potential of chronotherapeutic approaches for ischaemic heart disease.
{"title":"BMAL1 and HIF2α are key regulators of circadian-dependent variations in myocardial injury","authors":"Karina Huynh","doi":"10.1038/s41569-025-01169-4","DOIUrl":"10.1038/s41569-025-01169-4","url":null,"abstract":"A new study published in Nature reveals the role of the interaction between the circadian transcription factor BMAL1 and hypoxia-inducible factor 2α in circadian-dependent cardioprotection after ischaemia–reperfusion injury, and highlights the potential of chronotherapeutic approaches for ischaemic heart disease.","PeriodicalId":18976,"journal":{"name":"Nature Reviews Cardiology","volume":"22 7","pages":"464-464"},"PeriodicalIF":44.2,"publicationDate":"2025-05-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143933468","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 : 2025-05-09DOI: 10.1038/s41569-025-01162-x
Alessandra Pasut, Eleonora Lama, Amaryllis H. Van Craenenbroeck, Jeffrey Kroon, Peter Carmeliet
Endothelial cells are multifunctional cells that form the inner layer of blood vessels and have a crucial role in vasoreactivity, angiogenesis, immunomodulation, nutrient uptake and coagulation. Endothelial cells have unique metabolism and are metabolically heterogeneous. The microenvironment and metabolism of endothelial cells contribute to endothelial cell heterogeneity and metabolic specialization. Endothelial cell dysfunction is an early event in the development of several cardiovascular diseases and has been shown, at least to some extent, to be driven by metabolic changes preceding the manifestation of clinical symptoms. Diabetes mellitus, hypertension, obesity and chronic kidney disease are all risk factors for cardiovascular disease. Changes in endothelial cell metabolism induced by these cardiometabolic stressors accelerate the accumulation of dysfunctional endothelial cells in tissues and the development of cardiovascular disease. In this Review, we discuss the diversity of metabolic programmes that control endothelial cell function in the cardiovascular system and how these metabolic programmes are perturbed in different cardiovascular diseases in a disease-specific manner. Finally, we discuss the potential and challenges of targeting endothelial cell metabolism for the treatment of cardiovascular diseases. In this Review, the authors describe the metabolic programmes that control endothelial cell function in the cardiovascular system, discuss the role of endothelial cell metabolism in different cardiovascular diseases, and highlight the therapeutic potential and challenges of targeting endothelial cell metabolism to treat cardiovascular diseases.
{"title":"Endothelial cell metabolism in cardiovascular physiology and disease","authors":"Alessandra Pasut, Eleonora Lama, Amaryllis H. Van Craenenbroeck, Jeffrey Kroon, Peter Carmeliet","doi":"10.1038/s41569-025-01162-x","DOIUrl":"10.1038/s41569-025-01162-x","url":null,"abstract":"Endothelial cells are multifunctional cells that form the inner layer of blood vessels and have a crucial role in vasoreactivity, angiogenesis, immunomodulation, nutrient uptake and coagulation. Endothelial cells have unique metabolism and are metabolically heterogeneous. The microenvironment and metabolism of endothelial cells contribute to endothelial cell heterogeneity and metabolic specialization. Endothelial cell dysfunction is an early event in the development of several cardiovascular diseases and has been shown, at least to some extent, to be driven by metabolic changes preceding the manifestation of clinical symptoms. Diabetes mellitus, hypertension, obesity and chronic kidney disease are all risk factors for cardiovascular disease. Changes in endothelial cell metabolism induced by these cardiometabolic stressors accelerate the accumulation of dysfunctional endothelial cells in tissues and the development of cardiovascular disease. In this Review, we discuss the diversity of metabolic programmes that control endothelial cell function in the cardiovascular system and how these metabolic programmes are perturbed in different cardiovascular diseases in a disease-specific manner. Finally, we discuss the potential and challenges of targeting endothelial cell metabolism for the treatment of cardiovascular diseases. In this Review, the authors describe the metabolic programmes that control endothelial cell function in the cardiovascular system, discuss the role of endothelial cell metabolism in different cardiovascular diseases, and highlight the therapeutic potential and challenges of targeting endothelial cell metabolism to treat cardiovascular diseases.","PeriodicalId":18976,"journal":{"name":"Nature Reviews Cardiology","volume":"22 12","pages":"923-943"},"PeriodicalIF":44.2,"publicationDate":"2025-05-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143930876","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 : 2025-05-08DOI: 10.1038/s41569-025-01164-9
Ritu Thamman, Rafael Vidal-Perez
Digital communication increasingly shapes early-career cardiology. Social media offers powerful tools for education, networking and career growth, but also poses challenges such as misinformation and lack of professionalism. In this Comment article, we outline practical strategies for effectively navigating social media in the early stages of a cardiology career.
{"title":"Social media in modern cardiology: a tool for building community, visibility and impact","authors":"Ritu Thamman, Rafael Vidal-Perez","doi":"10.1038/s41569-025-01164-9","DOIUrl":"10.1038/s41569-025-01164-9","url":null,"abstract":"Digital communication increasingly shapes early-career cardiology. Social media offers powerful tools for education, networking and career growth, but also poses challenges such as misinformation and lack of professionalism. In this Comment article, we outline practical strategies for effectively navigating social media in the early stages of a cardiology career.","PeriodicalId":18976,"journal":{"name":"Nature Reviews Cardiology","volume":"22 7","pages":"457-458"},"PeriodicalIF":44.2,"publicationDate":"2025-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143920220","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 : 2025-05-06DOI: 10.1038/s41569-025-01160-z
Clément Menuet, Alona Ben-Tal, Ambre Linossier, Andrew M. Allen, Benedito H. Machado, Davi J. A. Moraes, David G. S. Farmer, David J. Paterson, David Mendelowitz, Edward G. Lakatta, Edwin W. Taylor, Gareth L. Ackland, Irving H. Zucker, James P. Fisher, James S. Schwaber, Julia Shanks, Julian F. R. Paton, Julie Buron, K. Michael Spyer, Kalyanam Shivkumar, Mathias Dutschmann, Michael J. Joyner, Neil Herring, Paul Grossman, Robin M. McAllen, Rohit Ramchandra, Song T. Yao, Thomas Ritz, Alexander V. Gourine
The variation of heart rate in phase with breathing, known as ‘respiratory sinus arrhythmia’ (RSA), is a physiological phenomenon present in all air-breathing vertebrates. RSA arises from the interaction of several physiological mechanisms but is primarily mediated by rhythmic changes in cardiac parasympathetic (vagal) activity, increasing heart rate during inspiration and decreasing heart rate during expiration. RSA amplitude is an indicator of autonomic and cardiac health; RSA is diminished or absent in common pathological conditions such as chronic heart failure and hypertension. In this Expert Recommendation, we argue that the term ‘RSA’, although historically important, is semantically inaccurate and carries misleading pathological connotations, contributing to misunderstanding and misinterpretation of the origin and the physiological importance of the phenomenon. We propose replacing ‘RSA’ with the term ‘respiratory heart rate variability’ (RespHRV), which avoids pathological connotations and emphasizes the specific respiratory contribution to heart rate variability. We clarify that RespHRV encompasses respiratory-related heart rate variations in both the low-frequency and high-frequency bands traditionally defined in heart rate variability analysis, and that its amplitude should not be misconstrued as a measure of vagal tone. Adopting the proposed term ‘RespHRV’ is expected to unify understanding and stimulate further experimental and clinical research into the physiological mechanisms and functional importance of this phenomenon. The physiological phenomenon whereby heart rate varies in phase with breathing in vertebrates has been known as ‘respiratory sinus arrhythmia’. In this Expert Recommendation, the authors argue that this terminology is potentially misleading and propose replacing it with the term ‘respiratory heart rate variability’, which avoids pathological connotations.
{"title":"Redefining respiratory sinus arrhythmia as respiratory heart rate variability: an international Expert Recommendation for terminological clarity","authors":"Clément Menuet, Alona Ben-Tal, Ambre Linossier, Andrew M. Allen, Benedito H. Machado, Davi J. A. Moraes, David G. S. Farmer, David J. Paterson, David Mendelowitz, Edward G. Lakatta, Edwin W. Taylor, Gareth L. Ackland, Irving H. Zucker, James P. Fisher, James S. Schwaber, Julia Shanks, Julian F. R. Paton, Julie Buron, K. Michael Spyer, Kalyanam Shivkumar, Mathias Dutschmann, Michael J. Joyner, Neil Herring, Paul Grossman, Robin M. McAllen, Rohit Ramchandra, Song T. Yao, Thomas Ritz, Alexander V. Gourine","doi":"10.1038/s41569-025-01160-z","DOIUrl":"10.1038/s41569-025-01160-z","url":null,"abstract":"The variation of heart rate in phase with breathing, known as ‘respiratory sinus arrhythmia’ (RSA), is a physiological phenomenon present in all air-breathing vertebrates. RSA arises from the interaction of several physiological mechanisms but is primarily mediated by rhythmic changes in cardiac parasympathetic (vagal) activity, increasing heart rate during inspiration and decreasing heart rate during expiration. RSA amplitude is an indicator of autonomic and cardiac health; RSA is diminished or absent in common pathological conditions such as chronic heart failure and hypertension. In this Expert Recommendation, we argue that the term ‘RSA’, although historically important, is semantically inaccurate and carries misleading pathological connotations, contributing to misunderstanding and misinterpretation of the origin and the physiological importance of the phenomenon. We propose replacing ‘RSA’ with the term ‘respiratory heart rate variability’ (RespHRV), which avoids pathological connotations and emphasizes the specific respiratory contribution to heart rate variability. We clarify that RespHRV encompasses respiratory-related heart rate variations in both the low-frequency and high-frequency bands traditionally defined in heart rate variability analysis, and that its amplitude should not be misconstrued as a measure of vagal tone. Adopting the proposed term ‘RespHRV’ is expected to unify understanding and stimulate further experimental and clinical research into the physiological mechanisms and functional importance of this phenomenon. The physiological phenomenon whereby heart rate varies in phase with breathing in vertebrates has been known as ‘respiratory sinus arrhythmia’. In this Expert Recommendation, the authors argue that this terminology is potentially misleading and propose replacing it with the term ‘respiratory heart rate variability’, which avoids pathological connotations.","PeriodicalId":18976,"journal":{"name":"Nature Reviews Cardiology","volume":"22 12","pages":"978-984"},"PeriodicalIF":44.2,"publicationDate":"2025-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143915152","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 : 2025-04-28DOI: 10.1038/s41569-025-01152-z
Zachary L. Cox, Kevin Damman, Jeffrey M. Testani
Heart failure is a leading cause of hospitalization worldwide, and congestion is the predominant cause of heart failure symptoms and hospitalization. The primary therapy used to treat and prevent congestion has historically been loop diuretics. However, many patients are discharged from hospital with residual congestion, which is associated with persistent heart failure symptoms, adverse outcomes and hospital readmission. Multiple medical strategies and devices have been and are being investigated with the aim of improving decongestion and subsequent heart failure outcomes. Numerous questions exist about the design of clinical trials to test emerging medical and device therapies, including the magnitude of benefit on congestive, kidney and post-discharge outcomes relative to conventional decongestion practices, and how best to implement novel therapies. In this Review, we discuss emerging medical and device strategies targeting congestion in patients with heart failure. Congestion is the predominant cause of heart failure symptoms and hospitalization. In this Review, Testani and colleagues discuss established and emerging medical and device strategies to treat congestion and improve outcomes in patients with heart failure.
{"title":"Decongestion in heart failure: medical and device therapies","authors":"Zachary L. Cox, Kevin Damman, Jeffrey M. Testani","doi":"10.1038/s41569-025-01152-z","DOIUrl":"10.1038/s41569-025-01152-z","url":null,"abstract":"Heart failure is a leading cause of hospitalization worldwide, and congestion is the predominant cause of heart failure symptoms and hospitalization. The primary therapy used to treat and prevent congestion has historically been loop diuretics. However, many patients are discharged from hospital with residual congestion, which is associated with persistent heart failure symptoms, adverse outcomes and hospital readmission. Multiple medical strategies and devices have been and are being investigated with the aim of improving decongestion and subsequent heart failure outcomes. Numerous questions exist about the design of clinical trials to test emerging medical and device therapies, including the magnitude of benefit on congestive, kidney and post-discharge outcomes relative to conventional decongestion practices, and how best to implement novel therapies. In this Review, we discuss emerging medical and device strategies targeting congestion in patients with heart failure. Congestion is the predominant cause of heart failure symptoms and hospitalization. In this Review, Testani and colleagues discuss established and emerging medical and device strategies to treat congestion and improve outcomes in patients with heart failure.","PeriodicalId":18976,"journal":{"name":"Nature Reviews Cardiology","volume":"22 12","pages":"961-977"},"PeriodicalIF":44.2,"publicationDate":"2025-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143880706","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}