CIRCULATION循环
CIRCULATION(英文缩写 CIRCULATION),ISSN 0009-7322,eISSN 1524-4539,中文译名:循环 是一本学术期刊。本页汇总该期刊的最新影响因子、分区信息以及最新收录于 PubMed 的文献,帮助您快速了解期刊全貌。
发文量统计区间：2025-11-01 至 2026-10-31，按本站收录文献的发表日期统计。
期刊介绍
历年影响因子趋势
| JCR 数据年份 | 影响因子 | JCR 分区 |
|---|---|---|
| 2021 | 39.922 | Q1 |
| 2022 | 37.800 | Q1 |
| 2023 | 35.500 | Q1 |
| 2024 | 38.600 | Q1 |
| 2025 | 41.300 | Q1 |
CIRCULATION 最新收录文献
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1. Epigenome-Wide Association Study of Abdominal Aortic Aneurysm Identifies Central Role for Inflammatory Pathways.
1. 腹主动脉瘤的表观基因组广泛关联研究揭示了炎症通路的中心作用。PMID:日期:2026-09-29Epigenetic mechanisms underlying susceptibility to abdominal aortic aneurysm (AAA) remain poorly understood. Identifying causal DNA methylation markers for AAA can elucidate the regulatory processes that drive aneurysm formation and accelerate translational applications. We leveraged the Veterans Affairs (VA) Million Veteran Program to identify methylation biomarkers and delineate underlying pathways. We first conducted an epigenome-wide association study of incident AAA (1324 cases and 42 065 noncases), performed stratified analyses by population group and smoking status, and conducted Mendelian randomization to facilitate causal inference of the CpG-AAA association. Chromatin state, island context, and transcription factor binding were implicated through functional annotation of identified CpGs. To identify genes impacted by change in methylation state, we aligned associations with transcriptional data obtained in blood, aorta, and liver. We performed expression quantitative trait methylation to capture CpG-gene-expression links across the genome. Network Mendelian randomization was used to test cardiometabolic and inflammatory mediation. Finally, we developed a methylation risk score for AAA using penalized regression and evaluated its performance against a clinical model in the Million Veteran Program and 2 external studies. Epigenome-wide association study identified 1253 CpGs associated with incident AAA, and Mendelian randomization supported a putative causal role for 143 of these associations. Functional annotation pointed to predominantly distal, enhancer-centered regulation and enrichment of inflammatory transcription factor programs (eg, activator protein-1 and nuclear factor κB). This distal architecture was consistent with expression quantitative trait methylation results, which showed a larger number of trans associations. Among 143 CpGs associated with AAA in Mendelian randomization analyses, we identified 213 CpG-gene expression pairs with strong colocalization support, including , and . Multi-trait colocalization further prioritized 8 CpG-gene expression-AAA links with evidence of a shared genetic signal. Network Mendelian randomization identified 135 putative mediation pathways linking CpGs to AAA, including 58 via cardiometabolic traits and 77 via inflammation-related traits. Blood lipid traits mediated >40% of the associations between AAA risk and CpGs near (cg19305903) and (cg14128479). Among inflammation-related mediators, circulating DAG1, NEXN, MMP9, IL1RN, and MMP13 were prioritized as potential intermediates. Additionally, a CpG selection process was used to develop a methylation risk score for AAA, which strongly associated with disease in both the discovery cohort and 2 external validation cohorts, even after adjustment for a full suite of clinical covariates. This study identified putative causal DNA methylation markers for AAA, and multi-omics analyses implicate activator protein-1-linked inflammatory transcriptional programs, blood lipids, and multiple inflammation-related proteins as key pathways underlying methylation-associated AAA risk.
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2. From Hippocrates to Biologics, The Evolving History of Pericarditis: A Review.
PMID:日期:2026-09-28Pericarditis remains a common and clinically relevant cardiovascular condition whose diagnosis and management have evolved substantially over time. Understanding this historical progression provides important context for contemporary practice and emerging therapeutic strategies. Early descriptions, dating back to Hippocrates, framed pericarditis as a clinical observation, with more precise diagnostic characterization emerging in the 19th century through the work of Laennec and later refined by clinicians such as Spodick and Hatle. Initial treatment approaches were largely symptomatic or surgical, including pericardiectomy for advanced constrictive disease. The mid-twentieth century marked a shift toward medical therapy with the introduction of nonsteroidal anti-inflammatory drugs and corticosteroids, which improved symptom control but were limited by high recurrence rates. The advent of echocardiography transformed pericardial disease evaluation by enabling noninvasive diagnosis, hemodynamic assessment, and safer pericardiocentesis. More recently, cardiac magnetic resonance imaging has further advanced care by allowing detailed tissue characterization and improved risk stratification. Randomized trials established colchicine as a cornerstone therapy for both acute and recurrent pericarditis. A major paradigm shift has occurred with the recognition of autoinflammatory mechanisms underlying recurrent disease and the introduction of targeted interleukin-1 inhibition, including anakinra and rilonacept, particularly for refractory cases. Together, these advances reflect a transition from empirical management toward mechanism-based, personalized care. Ongoing progress in imaging, biomarker integration, and targeted immunomodulation is expected to further refine diagnosis, treatment, and long-term outcomes for patients with pericardial disease.
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3. 2026 AHA/ACC/ACS/ASNC/HRS/SCA/SCCT/SCMR/SVM Guideline for Perioperative Cardiovascular Management for Noncardiac Surgery: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines.
3. 2026 AHA/ACC/ACS/ASNC/HRS/SCA/SCCT/SCMR/SVM非心脏手术围手术期心血管管理指南：美国心脏病学会/美国心脏协会临床实践指南联合委员会报告PMID:日期:2026-09-28The "2026 AHA/ACC/ACS/ASNC/HRS/SCA/SCCT/SCMR/SVM Guideline for Perioperative Cardiovascular Management for Noncardiac Surgery" provides recommendations to guide clinicians in the perioperative cardiovascular evaluation and management of adult patients undergoing noncardiac surgery. A comprehensive literature search was conducted from August 2022 to March 2023 to identify clinical studies, reviews, and other evidence conducted on human subjects that were published in English from MEDLINE (through PubMed), EMBASE, the Cochrane Library, the Agency for Healthcare Research and Quality, and other selected databases relevant to this guideline. Recommendations from the "2014 ACC/AHA Guideline on Perioperative Cardiovascular Evaluation and Management of Patients Undergoing Noncardiac Surgery" have been updated with new evidence consolidated to guide clinicians; clinicians should be advised this guideline supersedes the previously published 2014 guideline. In addition, evidence-based management strategies, including pharmacological therapies, perioperative monitoring, and devices, for cardiovascular disease and associated medical conditions, have been developed.
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4. Modeling Heart Failure With Preserved Ejection Fraction Using Human Induced Pluripotent Stem Cell-Derived Cardiomyocytes.
4. 利用人诱导多能干细胞衍生的心肌细胞构建射血分数保留型心力衰竭模型PMID:日期:2026-09-28该文献暂无摘要。
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5. Response by Yang et al to Letter Regarding Article, "Association of Pre-Fontan Hemodynamics With Long-Term Outcomes After Fontan Palliation: A Study From the Pediatric Cardiac Care Consortium".
5. Yang等人对关于文章“Fontan术前血流动力学与Fontan姑息术后长期结局的关联：来自儿科心脏护理联盟的研究”的来信的回复PMID:日期:2026-09-28该文献暂无摘要。
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6. Sotatercept Improves Right Heart Mechanics Despite Reduced Myocardial Contractility in Pulmonary Arterial Hypertension: A Prospective Exercise Hemodynamic Study.
6. Sotatercept改善肺动脉高压患者右心力学但降低心肌收缩力：一项前瞻性运动血流动力学研究PMID:日期:2026-09-22The right ventricular (RV) response to pressure overload is a crucial determinant of outcomes in pulmonary arterial (PA) hypertension. Sotatercept improves clinical outcomes, but its effects on the right ventricle have been inconsistent. We evaluated the effects of sotatercept on load-independent measures of RV contractility, RV-PA coupling, and right heart deformation at rest and exertion in patients with PA hypertension. In this prospective trial among participants with PA hypertension recruited between July 2024 and May 2025, we performed simultaneous echocardiography and invasive pressure measurements during rest and exercise to evaluate changes in RV contractility (end-systolic elastance [Ees]), afterload (PA elastance [Ea]), RV-PA coupling (ratio of arterial Ea to Ees), and right heart deformation, including RV and right atrial strain, before and after 24 weeks of sotatercept using mixed models. Among 30 participants (n=21; 70% female; mean age, 49.3 years [SD 13.5]), sotatercept decreased PA Ea. These changes were associated with reduced RV contractility, PA pulsatility index, and the maximal rate of RV pressure increase over time (dP/dt; <0.001 for all). The decrease in Ees was associated with a decrease in PA Ea (r=+0.70 [95% CI, +0.44 to +0.85]; <0.0001) with preserved RV-PA coupling (mean difference, +0.08 [95% CI, -0.11 to +0.26]; =0.42). Although systolic indices measured at the base of the right ventricle (tricuspid annular plane systolic excursion and systolic velocity of the lateral tricuspid annulus) decreased after sotatercept use, there was an increase in RV free wall-dependent systolic indices, including resting and exercise RV free wall strain (mean difference, +6.2% [95% CI, +4.5 to +7.8]; <0.0001) and fractional area change (=0.0001). Beyond the right ventricle, there was also improved right atrial filling and contractile performance across rest and exercise (<0.0001 for all). Sotatercept decreases RV contractility in proportion to reduced afterload, while preserving the RV-PA coupling relationship. Despite decreased RV contractility, global measures of right heart performance, such as RV free wall strain and RA strain, improve, alongside redistribution of RV deformation from annular motion to free wall shortening. These data suggest that sotatercept causes an energetically favorable reduction in resting RV contractility to match the lower afterload, which does not appear physiologically detrimental when considering the concurrent improvement in RV free wall contractile mechanics and exertional right heart reserve. URL: https://www.clinicaltrials.gov; Unique identifier: NCT06409026.
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7. Real-World Experience With the Extravascular Implantable Cardioverter Defibrillator Through 1 Year: The Enlighten Post Approval Registry Study.
7. 血管外植入式心律转复除颤器一年期真实世界应用经验：Enlighten上市后批准注册研究PMID:日期:2026-09-22The extravascular implantable cardioverter defibrillator (EV-ICD) was developed to provide defibrillation and antitachycardia pacing therapy without the need for intravascular lead placement. Premarket clinical trials reported EV-ICD safety and efficacy through 3 years, but a real-world assessment of the Aurora EV-ICD system, which includes a novel sensing discriminator, is needed. The objective of this analysis was to assess real-world therapy efficacy and safety of the EV-ICD through 1 year. Enlighten: The EV-ICD Post Approval Registry is a prospective, global, real-world registry that included patients who underwent an EV-ICD implantation attempt. The main safety analysis was freedom from all system- or procedure-related major complications through 1 year. Event rates at 1 year were calculated using the Kaplan-Meier method. EV-ICD system implantation was attempted by 168 implanters in 787 patients (49.1±15.2 years old; 28.7% women; 34.1% secondary prevention). Tunneling and lead placement in the substernal space were achieved in 781 of 787 patients (99.2%), with 758 patients (96.3%) remaining implanted following defibrillation and electrical testing. One-year freedom from major system- or procedure-related complications was 89.1% (95% CI, 86.3%-91.3%). The 1-year rate of first appropriate therapy (shock, antitachycardia pacing, or both) was 7.3% (95% CI, 5.5-9.6). Shock success for discrete spontaneous episodes was 100% (61 of 61), and the generalized estimating equations antitachycardia pacing success rate, to account for multiple episodes per patient, was 74.2% for monomorphic ventricular tachycardia. The 1-year rate of first inappropriate shock was 7.1% (95% CI, 5.4-9.4), with noncardiac oversensing as the main cause (40.5% of inappropriately shocked episodes). In the largest prospective worldwide cohort of patients with an EV-ICD to date, both antitachycardia pacing and shock therapy were effective, while the rate of major complications agreed with the premarket experience through 1 year. These data demonstrate that positive outcomes of the EV-ICD are retained in everyday clinical practice in a large, global cohort with an expanded number of implanters. URL: https://www.clinicaltrials.gov; Unique identifier: NCT06048731.
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8. Prognostic Value of Coronary Computed Tomography Angiography-Derived Fractional Flow Reserve From a Large Nationwide Cohort.
8. 来自全国大型队列的冠状动脉计算机断层扫描血管造影衍生血流储备分数的预后价值PMID:日期:2026-09-22The diagnostic value of coronary computed tomography angiography-derived fractional flow reserve (FFR-CT) in stable coronary artery disease is well established. The prognostic value of predicting future cardiovascular events is less clear, as studies are limited by small populations, variable measurement points, composite outcomes, and short follow-up. A nationwide cohort of coronary computed tomography angiography with 3-year follow-up was used to examine the association between FFR-CT measurements and future cardiovascular events. Patients receiving coronary computed tomography angiography and clinically indicated FFR-CT analysis (HeartFlow) for stable coronary artery disease between 2017 and 2020 at 27 sites across England were included. Lowest per-patient stenosis-specific and distal vessel FFR-CT measurements were related to individual outcomes of myocardial infarction (MI), cardiovascular mortality, all-cause mortality, and revascularization. FFR-CT measurements were divided into subgroups to investigate for a gradient of risk: normal FFR-CT (>0.8), borderline (0.71-0.8), reduced (0.51-0.7), and severely reduced (≤0.5). In total, 7836 patients aged 63 (56.0-71.0), 37.4% women, underwent FFR-CT analysis. Stenosis-specific FFR-CT was associated with future MI (hazard ratio [HR], 2.08-5.73; <0.001), cardiovascular death (HR, 1.51-3.40; <0.001), all-cause death (HR, 1.01-1.58; =0.01), and revascularization (HR, 4.79-24.48; <0.001), with lower FFR-CT values associated with incrementally greater risk. After adjusting for cardiovascular risk factors and coronary stenosis severity (Coronary Artery Disease Reporting and Data System), stenosis-specific FFR-CT≤0.7 was associated with MI (adjusted HR, 2.94-3.39; <0.001), ≤0.5 with cardiovascular death (adjusted HR, 2.92; =0.02), all-cause death (adjusted HR, 1.49; =0.045), and ≤0.8 with revascularization (adjusted HR, 3.02-9.42; <0.001). The addition of FFR-CT improved discrimination for MI or cardiovascular death compared with a risk factor and stenosis severity model (C index, 0.783; ∆C index, 0.012; <0.001). An FFR-CT value of 0.67 defined the optimal cutoff for risk of future cardiovascular events. Distal-vessel FFR-CT was associated with outcomes similar to stenosis-specific FFR-CT. Stenosis-specific and distal-vessel FFR-CT discordance was common (36.4%), but when stenosis-specific FFR-CT was normal, event rates were low (1.5% at 3 years for MI or cardiovascular death). FFR-CT is associated with the individual outcomes of MI, cardiovascular death, and all-cause death independent of risk factors and stenosis severity, with lower FFR-CT values associated with worse outcomes. Reduced and severely reduced FFR-CT have the strongest association with future cardiovascular events, with a value of 0.67 defining the optimal risk threshold.
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9. Novel mTORC1 Booster LAPTM4A Potentiates Pathological Cardiac Hypertrophy.
9. 新型mTORC1增强子LAPTM4A加剧病理性心肌肥厚PMID:日期:2026-09-22Excessive unnecessary protein accumulation in cardiomyocyte is a leading contributor for pathological cardiac hypertrophy and has been found closely regulated by the mTORC1 (mechanistic target of rapamycin complex 1) signaling and lysosome transmembrane proteins. However, the precise regulatory mechanism stratifying mTORC1 signaling and the specific functions of lysosomal proteins in protein homeostasis of cardiomyocytes remain largely unidentified. We screened lysosomal genes conserved in mice, rats, and humans. Adenoviral infection of rat cardiomyocytes was used to assess the functional role of LAPTM4A (lysosome-associated protein transmembrane 4A). To evaluate its effects in vivo, adeno-associated virus 9 driven by the cardiac troponin T promoter was used for cardiomyocyte-specific expression. RNA sequencing and mass spectrometry-based proteomics were performed to elucidate the underlying molecular mechanisms. Last, a dual-luciferase reporter assay was used to screen a Food and Drug Administration-approved drug library for compounds that suppress LAPTM4A expression. Lysosomal transmembrane proteins expressed in cardiomyocytes were screened for their roles in regulating hypertrophy, and LAPTM4A emerged as a potent promoter of cardiomyocyte hypertrophy and prohypertrophic gene expression. Overexpression of LAPTM4A aggravated cardiac remodeling and dysfunction by enhancing mTORC1-p70S6K (70-kDa ribosomal protein S6 kinase)/4EBP1 (eukaryotic translation initiation factor 4E-binding protein 1)-mediated protein synthesis, without affecting lysosomal autophagy, in a NEDD4L (neural precursor cell expressed developmentally downregulated 4-like)-dependent manner. Mechanistically, LAPTM4A directly interacted with NEDD4L, facilitating K63-linked ubiquitination of AKT (protein kinase B [v-akt murine thymoma viral oncogene homolog]) and subsequent activation of mTORC1 signaling. Cardiomyocyte-specific deletion of LAPTM4A significantly attenuated myocardial hypertrophy and fibrosis induced by transverse aortic constriction in mice. Furthermore, a dual-luciferase reporter screen identified magnolol, a Food and Drug Administration-approved compound, as a suppressor of LAPTM4A expression with marked cardioprotective effects in vivo. Our study identified a novel mTORC1 booster LAPTM4A and verified interrupting the LAPTM4A-mTORC1 axis can significantly inhibit excessive protein synthesis and pathological cardiac hypertrophy, which might represent an attractive therapeutic approach for this disease.
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10. {"_":"ALKBH5-Dependent mA Demethylation Promotes Cardiac Aging Through SLC38A3 Reduction and Glutamine Metabolic Alteration.","sup":["6"]}
10. {"_":"ALKBH5依赖的mA去甲基化通过SLC38A3减少和谷氨酰胺代谢改变促进心脏衰老。","sup":["6"]}PMID:日期:2026-09-22-methyladenosine (mA) modification has been linked to various types of physiological and pathological bioprocesses. However, the exact role of mA mRNA methylation in cardiac aging is largely unknown. Here, we show that ALKBH5 (alpha-ketoglutarate-dependent dioxygenase AlkB homolog 5), an mA demethylase, plays a critical role in regulating cardiac aging. Physiologically aged and paraquat-induced mouse models of cardiac aging as well as senescent cardiomyocyte cell cultures were used to evaluate the expression and function of ALKBH5 in cardiac aging. The adeno-associated virus serotype 9 and small interfering RNAs were used to modulate ALKBH5 expression in vivo and in vitro, respectively. Cardiac aging and function were evaluated by histological analysis, immunostaining, and echocardiography. Methylated RNA immunoprecipitation sequencing and functional screening were performed to identify potential targets of ALKBH5 in regulating cardiac aging. ALKBH5 expression was increased in aged hearts and in senescent-like cardiomyocyte models, accompanied by reduced mA levels. ALKBH5 knockdown attenuated senescence-associated phenotypes in cardiomyocytes and reduced aging-associated cardiac remodeling and dysfunction in physiological aging and paraquat-challenged mouse models when adeno-associated virus serotype 9-short hairpin RNA targeting ALKBH5 gene was delivered beginning in young adulthood, whereas ALKBH5 knockdown initiated in already aged hearts did not reverse established phenotypes. Mechanistically, ALKBH5-dependent mA demethylation reduced the expression of SLC38A3 (solute carrier family 38-member 3), which suggested a YTHDC2 (YTH domain-containing protein 2)-dependent mechanism, thereby contributing to reduced glutamine accumulation, impaired mitochondrial homeostasis, and increased oxidative stress. SLC38A3 overexpression attenuated aging-associated cardiac phenotypes in vivo. In addition, glutamine supplementation reduced senescence-associated and cardiac aging-related phenotypes. Our study demonstrates that ALKBH5-SLC38A3 axis is an important regulator of mA-linked, glutamine-associated pathways in aging-related cardiac phenotypes. These findings support a role for ALKBH5 as a contributor to cardiac aging-associated remodeling and dysfunction and suggest this pathway as a candidate target for further mechanistic and translational investigation.