Pub Date : 2024-06-25DOI: 10.1038/s41569-024-01053-7
Leonid Maizels, Jonathan M. Kalman
The advent of pulsed-field ablation — a series of ultra-rapid, high-energy pulses that result in non-thermal cell death via electroporation — is revolutionizing the field of atrial fibrillation ablation. Data on first iterations of the technology indicate that safety and efficacy are at least similar to that of thermal ablation but with meaningfully shorter procedure duration.
{"title":"Pulsed-field ablation: a revolution in atrial fibrillation therapy","authors":"Leonid Maizels, Jonathan M. Kalman","doi":"10.1038/s41569-024-01053-7","DOIUrl":"10.1038/s41569-024-01053-7","url":null,"abstract":"The advent of pulsed-field ablation — a series of ultra-rapid, high-energy pulses that result in non-thermal cell death via electroporation — is revolutionizing the field of atrial fibrillation ablation. Data on first iterations of the technology indicate that safety and efficacy are at least similar to that of thermal ablation but with meaningfully shorter procedure duration.","PeriodicalId":18976,"journal":{"name":"Nature Reviews Cardiology","volume":null,"pages":null},"PeriodicalIF":41.7,"publicationDate":"2024-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141450968","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 : 2024-06-19DOI: 10.1038/s41569-024-01054-6
Zuzanna Jablonska
In this Tools of the Trade article, Jablonska describes the use of proximity-based labelling for the proteomic profiling of novel protein–protein interactions.
{"title":"Proximity-based labelling for proteomic mapping","authors":"Zuzanna Jablonska","doi":"10.1038/s41569-024-01054-6","DOIUrl":"10.1038/s41569-024-01054-6","url":null,"abstract":"In this Tools of the Trade article, Jablonska describes the use of proximity-based labelling for the proteomic profiling of novel protein–protein interactions.","PeriodicalId":18976,"journal":{"name":"Nature Reviews Cardiology","volume":null,"pages":null},"PeriodicalIF":41.7,"publicationDate":"2024-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141427285","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 : 2024-06-19DOI: 10.1038/s41569-024-01055-5
Bronwyn Berkeley, Adrian Thomson
In this Tools of the Trade article, Berkeley and Thomson describe the use of a minimally invasive strategy to standardize the induction of myocardial infarction in mice.
在这篇 "贸易工具 "文章中，伯克利和汤姆森介绍了使用微创策略标准化诱导小鼠心肌梗死的方法。
{"title":"Suture-to-scan: ultrasonography-guided induction of heart injury","authors":"Bronwyn Berkeley, Adrian Thomson","doi":"10.1038/s41569-024-01055-5","DOIUrl":"10.1038/s41569-024-01055-5","url":null,"abstract":"In this Tools of the Trade article, Berkeley and Thomson describe the use of a minimally invasive strategy to standardize the induction of myocardial infarction in mice.","PeriodicalId":18976,"journal":{"name":"Nature Reviews Cardiology","volume":null,"pages":null},"PeriodicalIF":41.7,"publicationDate":"2024-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141425173","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 : 2024-06-12DOI: 10.1038/s41569-024-01051-9
Karina Huynh
Findings from a new study published in Science Immunology suggest that epigenetic changes in haematopoietic stem cells promote the production of pro-inflammatory macrophages and influence their capacity to generate protective macrophage subsets.
{"title":"Epigenetic changes in HSCs contribute to HF and comorbidities","authors":"Karina Huynh","doi":"10.1038/s41569-024-01051-9","DOIUrl":"10.1038/s41569-024-01051-9","url":null,"abstract":"Findings from a new study published in Science Immunology suggest that epigenetic changes in haematopoietic stem cells promote the production of pro-inflammatory macrophages and influence their capacity to generate protective macrophage subsets.","PeriodicalId":18976,"journal":{"name":"Nature Reviews Cardiology","volume":null,"pages":null},"PeriodicalIF":41.7,"publicationDate":"2024-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141309108","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 : 2024-06-07DOI: 10.1038/s41569-024-01052-8
Gregory B. Lim
Data from the phase IIb MUIR and ARCHES-2 trials show that RNA interference approaches that target either apolipoprotein C-III or ANGPTL3 significantly reduce plasma triglyceride levels in patients with mixed hyperlipidaemia.
{"title":"RNA interference lowers triglyceride levels","authors":"Gregory B. Lim","doi":"10.1038/s41569-024-01052-8","DOIUrl":"10.1038/s41569-024-01052-8","url":null,"abstract":"Data from the phase IIb MUIR and ARCHES-2 trials show that RNA interference approaches that target either apolipoprotein C-III or ANGPTL3 significantly reduce plasma triglyceride levels in patients with mixed hyperlipidaemia.","PeriodicalId":18976,"journal":{"name":"Nature Reviews Cardiology","volume":null,"pages":null},"PeriodicalIF":41.7,"publicationDate":"2024-06-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141288339","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 : 2024-06-05DOI: 10.1038/s41569-024-01048-4
Milda Folkmanaite, Manuela Zaccolo
Milda Folkmanaite and Manuela Zaccolo highlight a study that demonstrates a role for phase-separated condensates of protein kinase A in buffering molecules of cAMP, to illustrate how phase separation of proteins in cardiac cells might contribute to the regulation of cardiac function.
Milda Folkmanaite 和 Manuela Zaccolo 重点介绍了一项研究，该研究证明了蛋白激酶 A 的相分离凝聚物在缓冲 cAMP 分子中的作用，从而说明了心脏细胞中蛋白质的相分离可能有助于调节心脏功能。
{"title":"Phase separation of protein kinase A: a new paradigm in cardiac regulation?","authors":"Milda Folkmanaite, Manuela Zaccolo","doi":"10.1038/s41569-024-01048-4","DOIUrl":"10.1038/s41569-024-01048-4","url":null,"abstract":"Milda Folkmanaite and Manuela Zaccolo highlight a study that demonstrates a role for phase-separated condensates of protein kinase A in buffering molecules of cAMP, to illustrate how phase separation of proteins in cardiac cells might contribute to the regulation of cardiac function.","PeriodicalId":18976,"journal":{"name":"Nature Reviews Cardiology","volume":null,"pages":null},"PeriodicalIF":41.7,"publicationDate":"2024-06-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141262455","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 : 2024-06-05DOI: 10.1038/s41569-024-01049-3
Corey McAleese
Corey McAleese describes the study that identified the presence of metabolic heterogeneity in endothelial cells from different tissues and discusses its relevance to our current understanding of endothelial metabolism.
{"title":"Insights into endothelial metabolic heterogeneity","authors":"Corey McAleese","doi":"10.1038/s41569-024-01049-3","DOIUrl":"10.1038/s41569-024-01049-3","url":null,"abstract":"Corey McAleese describes the study that identified the presence of metabolic heterogeneity in endothelial cells from different tissues and discusses its relevance to our current understanding of endothelial metabolism.","PeriodicalId":18976,"journal":{"name":"Nature Reviews Cardiology","volume":null,"pages":null},"PeriodicalIF":41.7,"publicationDate":"2024-06-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141262454","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 : 2024-06-05DOI: 10.1038/s41569-024-01050-w
Daisy Jones
Haemophilia A is caused by variants in the gene that encodes coagulation factor VIII (FVIII). Sequencing of this gene in the 1980s was the initial step in developing replacement therapy with recombinant FVIII, and thereby removing the risk of blood-borne infections from plasma-derived FVIII.
{"title":"Characterization of the F8 gene: a silver lining in a dark cloud","authors":"Daisy Jones","doi":"10.1038/s41569-024-01050-w","DOIUrl":"10.1038/s41569-024-01050-w","url":null,"abstract":"Haemophilia A is caused by variants in the gene that encodes coagulation factor VIII (FVIII). Sequencing of this gene in the 1980s was the initial step in developing replacement therapy with recombinant FVIII, and thereby removing the risk of blood-borne infections from plasma-derived FVIII.","PeriodicalId":18976,"journal":{"name":"Nature Reviews Cardiology","volume":null,"pages":null},"PeriodicalIF":41.7,"publicationDate":"2024-06-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141251677","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 : 2024-05-30DOI: 10.1038/s41569-024-01038-6
David Bode, Julius Ryan D. Pronto, Gabriele G. Schiattarella, Niels Voigt
Atrial fibrillation (AF) is a continually growing health-care burden that often presents together with metabolic disorders, including diabetes mellitus and obesity. Current treatments often fall short of preventing AF and its adverse outcomes. Accumulating evidence suggests that metabolic disturbances can promote the development of AF through structural and electrophysiological remodelling, but the underlying mechanisms that predispose an individual to AF are aetiology-dependent, thus emphasizing the need for tailored therapeutic strategies to treat AF that target an individual’s metabolic profile. AF itself can induce changes in glucose, lipid and ketone metabolism, mitochondrial function and myofibrillar energetics (as part of a process referred to as ‘metabolic remodelling’), which can all contribute to atrial dysfunction. In this Review, we discuss our current understanding of AF in the setting of metabolic disorders, as well as changes in atrial metabolism that are relevant to the development of AF. We also describe the potential of available and emerging treatment strategies to target metabolic remodelling in the setting of AF and highlight key questions and challenges that need to be addressed to improve outcomes in these patients. In this Review, the authors describe the changes in metabolism that predispose individuals to developing atrial fibrillation (AF) and highlight the potential of available and emerging therapeutic strategies that target metabolic remodelling to treat AF.
{"title":"Metabolic remodelling in atrial fibrillation: manifestations, mechanisms and clinical implications","authors":"David Bode, Julius Ryan D. Pronto, Gabriele G. Schiattarella, Niels Voigt","doi":"10.1038/s41569-024-01038-6","DOIUrl":"10.1038/s41569-024-01038-6","url":null,"abstract":"Atrial fibrillation (AF) is a continually growing health-care burden that often presents together with metabolic disorders, including diabetes mellitus and obesity. Current treatments often fall short of preventing AF and its adverse outcomes. Accumulating evidence suggests that metabolic disturbances can promote the development of AF through structural and electrophysiological remodelling, but the underlying mechanisms that predispose an individual to AF are aetiology-dependent, thus emphasizing the need for tailored therapeutic strategies to treat AF that target an individual’s metabolic profile. AF itself can induce changes in glucose, lipid and ketone metabolism, mitochondrial function and myofibrillar energetics (as part of a process referred to as ‘metabolic remodelling’), which can all contribute to atrial dysfunction. In this Review, we discuss our current understanding of AF in the setting of metabolic disorders, as well as changes in atrial metabolism that are relevant to the development of AF. We also describe the potential of available and emerging treatment strategies to target metabolic remodelling in the setting of AF and highlight key questions and challenges that need to be addressed to improve outcomes in these patients. In this Review, the authors describe the changes in metabolism that predispose individuals to developing atrial fibrillation (AF) and highlight the potential of available and emerging therapeutic strategies that target metabolic remodelling to treat AF.","PeriodicalId":18976,"journal":{"name":"Nature Reviews Cardiology","volume":null,"pages":null},"PeriodicalIF":41.7,"publicationDate":"2024-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141179443","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 : 2024-05-29DOI: 10.1038/s41569-024-01043-9
Karina Huynh
Poscablo and colleagues identify a distinct haematopoietic platelet differentiation pathway that is enriched in ageing mice, which results in platelets that are hyper-reactive compared with canonical platelet populations.
{"title":"A distinct platelet differentiation pathway is involved in age-related thrombocytosis","authors":"Karina Huynh","doi":"10.1038/s41569-024-01043-9","DOIUrl":"10.1038/s41569-024-01043-9","url":null,"abstract":"Poscablo and colleagues identify a distinct haematopoietic platelet differentiation pathway that is enriched in ageing mice, which results in platelets that are hyper-reactive compared with canonical platelet populations.","PeriodicalId":18976,"journal":{"name":"Nature Reviews Cardiology","volume":null,"pages":null},"PeriodicalIF":49.6,"publicationDate":"2024-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141176159","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}
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