Circulation research最新文献

{"title":"Smooth Muscle-Induced Endothelial Dysfunction in Obesity; Don't Just Blame the Middleman.","authors":"Fred S Lamb, Ryan J Stark","doi":"10.1161/CIRCRESAHA.125.327129","DOIUrl":"10.1161/CIRCRESAHA.125.327129","url":null,"abstract":"","PeriodicalId":10147,"journal":{"name":"Circulation research","volume":"137 6","pages":"829-831"},"PeriodicalIF":16.2,"publicationDate":"2025-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144944958","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}

{"title":"Early Post-MI Proinflammatory Cardiac Endothelial Cells Contribute to Disease.","authors":"Marco Cremonesi, Marinos Kallikourdis","doi":"10.1161/CIRCRESAHA.125.327127","DOIUrl":"https://doi.org/10.1161/CIRCRESAHA.125.327127","url":null,"abstract":"","PeriodicalId":10147,"journal":{"name":"Circulation research","volume":"137 6","pages":"880-881"},"PeriodicalIF":16.2,"publicationDate":"2025-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144944846","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}

{"title":"Meet the First Authors.","authors":"","doi":"10.1161/RES.0000000000000729","DOIUrl":"https://doi.org/10.1161/RES.0000000000000729","url":null,"abstract":"","PeriodicalId":10147,"journal":{"name":"Circulation research","volume":"137 6","pages":"809-811"},"PeriodicalIF":16.2,"publicationDate":"2025-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144944849","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}

{"title":"Interplay Between Ryanodine Receptor Arrangement and Function: Implications for (Patho)physiological Control of Calcium Release.","authors":"Luis A Gonano, Alycia M Kinns, Anna Bergan-Dahl, William E Louch, Peter P Jones","doi":"10.1161/CIRCRESAHA.125.325387","DOIUrl":"https://doi.org/10.1161/CIRCRESAHA.125.325387","url":null,"abstract":"<p><p>Calcium release through the cardiac RyR2 (type-2 ryanodine receptor) is essential for cardiac contraction. RyR2 dysfunction is associated with a spectrum of cardiac pathologies, most notably arrhythmias. While excessive RyR2 activity was historically seen as the driver of arrhythmia, it is now clear that inadequate calcium release is equally detrimental. This homeostatic balance of activity requires precise tuning, which is provided by a swathe of regulating factors spanning posttranslational modifications, protein-protein interactions, and the more recently identified positioning of individual RyR2 channels within the cell. This review summarizes how too much, or too little, calcium release can lead to arrhythmia and explores how the multitude of regulating factors work synergistically to set and modify RyR2 physiologically and become impaired in disease. Finally, we examine how RyR2-targeted pharmacological approaches can therapeutically rebalance calcium handling and inhibit arrhythmia.</p>","PeriodicalId":10147,"journal":{"name":"Circulation research","volume":"137 6","pages":"902-923"},"PeriodicalIF":16.2,"publicationDate":"2025-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144944862","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}

{"title":"RNA Therapeutics for In Vivo CAR-Macrophage: Advancing Cardiac Immunotherapy.","authors":"Soumaya Ben-Aicha, Talia A Shmool, Costanza Emanueli","doi":"10.1161/CIRCRESAHA.125.327128","DOIUrl":"https://doi.org/10.1161/CIRCRESAHA.125.327128","url":null,"abstract":"","PeriodicalId":10147,"journal":{"name":"Circulation research","volume":"137 6","pages":"860-862"},"PeriodicalIF":16.2,"publicationDate":"2025-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144944975","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}

{"title":"Spatio-Temporal Proliferative Heterogeneity of Intra-Organ Endothelial Cells.","authors":"Maoying Han,Zhicong Liu,Lei Liu,Zhixin Kang,Xiuzhen Huang,Nicola Smart,Xuekun Li,Qiang Shu,Bin Zhou","doi":"10.1161/circresaha.125.326748","DOIUrl":"https://doi.org/10.1161/circresaha.125.326748","url":null,"abstract":"BACKGROUNDBlood vessels play a crucial role in supplying tissues with oxygen and nutrients. The maintenance of normal blood vessel number and integrity requires a continuous supply of new endothelial cells (ECs) through self-replication. While it is established that ECs across different tissues exhibit heterogeneity in molecular signatures and regenerative capacities, the extent of proliferation heterogeneity among ECs within the same organ or tissue remains largely unexplored.METHODSAn EC-specific proliferation tracing system was developed to investigate the proliferative heterogeneity of ECs in the heart, liver, and lung. A combination of RNA sequencing, spatial transcriptomics, and single-cell RNA sequencing was used to uncover the underlying mechanisms of this heterogeneity. An MAPK signaling inhibitor was administered in vivo to functionally assess pathway involvement. Injury models, including transverse aortic constriction, myocardial infarction, partial hepatectomy, and pneumonectomy, were utilized to assess stress-induced EC proliferation.RESULTSEC proliferation exhibits marked intraorgan heterogeneity. In the heart, ECs in the upper part of the ventricular septum, the superior-inner left ventricle wall, and the apex showed elevated proliferation. In the liver, E-CAD (e-cadherin)±1 liver sinusoidal EC displayed a distinct proliferative advantage. In the lung, PLVAP (plasma membrane vesicle-associated protein)+ ECs renew more actively than CAR4 (carbonic anhydrase 4)+ ECs. Multiomics analysis revealed regional transcription diversity. In vivo MAPK inhibition confirmed its role in regulating EC proliferative heterogeneity.CONCLUSIONSThis study uncovers regional and subtype-specific proliferation in the heart, liver, and lung, driven by distinct gene expression programs. These findings highlight the spatial and functional diversity of microvascular ECs and offer a framework for developing organ-specific vascular regenerative strategies.","PeriodicalId":10147,"journal":{"name":"Circulation research","volume":"27 1","pages":""},"PeriodicalIF":20.1,"publicationDate":"2025-08-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144850881","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}

{"title":"Orphan Under Pressure: GPR146 as a Mechanotransduction Modulator.","authors":"Laena Pernomian,Juliana Montenegro Parente,Cameron G McCarthy,Camilla Ferreira Wenceslau","doi":"10.1161/circresaha.125.327056","DOIUrl":"https://doi.org/10.1161/circresaha.125.327056","url":null,"abstract":"","PeriodicalId":10147,"journal":{"name":"Circulation research","volume":"14 1","pages":"625-627"},"PeriodicalIF":20.1,"publicationDate":"2025-08-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144850885","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}

{"title":"Restless Legs Syndrome, Periodic Leg Movements, Hypertension and Cardiovascular Diseases.","authors":"Yves Dauvilliers,Sofiene Chenini,Lucie Barateau,Virend K Somers","doi":"10.1161/circresaha.125.325677","DOIUrl":"https://doi.org/10.1161/circresaha.125.325677","url":null,"abstract":"Restless legs syndrome (RLS) is a frequent sleep-related sensorimotor disorder defined by an urge to move the legs in the evening while resting. Severe RLS symptoms can negatively impact sleep, mood, and quality of life. Periodic leg movements during sleep and wakefulness are found in 60% to 80% of patients with RLS. The pathophysiology of RLS and periodic leg movement is still poorly understood and involves brain iron deficiency, dopamine dysregulation, and genetic predisposition. Over the past decades, several cross-sectional and longitudinal studies have reported an association between RLS, cardiovascular disease, and hypertension although the magnitude, direction, and underlying mechanisms of these associations remain inconclusive. Periodic leg movements during sleep are concomitant with an increase in blood pressure and heart rate, which may affect the physiological nocturnal blood pressure dip and, therefore, lead to an increased incidence of cardiovascular disease. Insomnia and sleep deprivation linked to sensory discomfort could also increase the sympathetic tone and contribute to an increase in cardiovascular risk. Comorbidities and associated sleep disorders may also synergically increase cardiovascular risk. This narrative review details the current knowledge of RLS, a still underdiagnosed and poorly recognized disorder, and examines the epidemiological relationship between RLS, cardiovascular disease and hypertension, potential mechanisms underlying this association, and strategies to reduce the risk of cardiovascular disease in patients with moderate-to-severe RLS. Greater multidisciplinary collaborations between cardiologists and sleep specialists are needed to better identify, understand, and manage patients with sleep disorders, including those with RLS.","PeriodicalId":10147,"journal":{"name":"Circulation research","volume":"39 1","pages":"746-763"},"PeriodicalIF":20.1,"publicationDate":"2025-08-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144850898","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}

{"title":"Insomnia Phenotypes, Cardiovascular Risk and Their Link to Brain Health.","authors":"Julio Fernandez-Mendoza","doi":"10.1161/circresaha.125.325686","DOIUrl":"https://doi.org/10.1161/circresaha.125.325686","url":null,"abstract":"About 30% to 40% of the general population experiences insomnia symptoms of difficulty initiating or maintaining sleep, and another 10% to 15% of the general population experiences chronic insomnia disorder. The prevalence of insomnia is disproportionately higher in people with cardiometabolic risk factors, cardiovascular diseases, cerebrovascular diseases, and neurocognitive disorders, including vascular cognitive impairment. In fact, recent meta-analytic evidence from epidemiological studies has demonstrated that insomnia, especially when accompanied by objective short sleep duration, is a risk factor for incident hypertension, type 2 diabetes, heart failure, stroke, cognitive impairment, Alzheimer disease, and all-cause mortality. Insomnia should, thus, be part of the prevention and management of these adverse health outcomes. However, randomized clinical trials have not demonstrated whether treatment with cognitive-behavioral therapy for insomnia, the first-line guideline-recommended treatment, or hypnotics/sedatives improves heart- or brain-related outcomes. Studies have also failed to consider insomnia a heterogeneous disorder consisting of distinct phenotypes that result from the relative contribution of biological versus cognitive-behavioral perpetuating factors. Objective short sleep duration has emerged as a marker of physiological hyperarousal in insomnia (ie, dysregulation of the hypothalamic-pituitary axis, increased sympathetic nervous system activation, and increased inflammation), as a predictor of insomnia-related adverse heart and brain health outcomes and, potentially, poor response to cognitive-behavioral therapy for insomnia. This review summarizes the meta-analytic evidence on the association of insomnia with cardiometabolic risk factors, cardiovascular diseases, cerebrovascular diseases, and neurocognitive disorders, including current knowledge on the heterogeneity of the disorder. This review also summarizes the potential pathophysiologic mechanisms that lead to heart and brain morbidity, which vary across insomnia phenotypes based on objective sleep duration. This review suggests that basic and clinical sciences need to unveil the molecular, cellular, and behavioral mechanisms at play across insomnia phenotypes, as the public health and clinical implications of their association with adverse heart and brain health are demanding immediate attention.","PeriodicalId":10147,"journal":{"name":"Circulation research","volume":"24 1","pages":"727-745"},"PeriodicalIF":20.1,"publicationDate":"2025-08-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144850888","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}

{"title":"Sleep Irregularity, Circadian Disruption, and Cardiometabolic Disease Risk.","authors":"Tianyi Huang","doi":"10.1161/circresaha.125.325613","DOIUrl":"https://doi.org/10.1161/circresaha.125.325613","url":null,"abstract":"Sleep irregularity, characterized by inconsistent sleep patterns from day to day, has become increasingly prevalent in today's 24/7 society. As a key component of multidimensional sleep health, the potential impact of sleep irregularity on cardiometabolic disease and mortality has recently received attention in research. In this review, we summarize the current evidence from epidemiological, clinical, and mechanistic studies to highlight the role of sleep irregularity in obesity, metabolic syndrome, diabetes, cardiovascular disease, and mortality. We focus on recent large prospective studies that establish stronger temporal relationships between sleep irregularity and cardiometabolic disease risk and mortality, compared with earlier cross-sectional studies. The preponderance of evidence supports that sleep irregularity is a robust risk factor for these conditions, and in some cases, may be a more significant predictor than other widely studied sleep factors, such as sleep duration. We propose potential biological, behavioral, and psychological pathways through which sleep irregularity may contribute to the development of cardiometabolic disease. We also discuss key limitations in the current literature, including the lack of standardized measures for assessing sleep irregularity, the scarcity of intervention studies to clarify its real-world implications, and the incomplete understanding of the underlying mechanisms. Addressing these gaps through further studies could pave the way for more effective clinical and public health strategies aimed at reducing sleep irregularity and ultimately mitigating the risk of cardiometabolic diseases and mortality.","PeriodicalId":10147,"journal":{"name":"Circulation research","volume":"70 1","pages":"709-726"},"PeriodicalIF":20.1,"publicationDate":"2025-08-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144850910","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}