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：2025-09-27 至 2026-09-27，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
-
1. Sotatercept Improves Right Heart Mechanics Despite Reduced Myocardial Contractility in Pulmonary Arterial Hypertension: A Prospective Exercise Hemodynamic Study.
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.
-
2. Real-World Experience With the Extravascular Implantable Cardioverter Defibrillator Through 1 Year: The Enlighten Post Approval Registry Study.
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.
-
3. Prognostic Value of Coronary Computed Tomography Angiography-Derived Fractional Flow Reserve From a Large Nationwide Cohort.
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.
-
4. Novel mTORC1 Booster LAPTM4A Potentiates Pathological Cardiac Hypertrophy.
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.
-
5. {"_":"ALKBH5-Dependent mA Demethylation Promotes Cardiac Aging Through SLC38A3 Reduction and Glutamine Metabolic Alteration.","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.
-
6. Asb2-KIF11 Axis Protects Against Heart Failure by Restoring Lysosomal Distribution and Mitochondrial Homeostasis.
PMID:日期:2026-09-22Heart failure remains a leading cause of mortality globally, driven by persistent mitochondrial dysfunction and maladaptive cardiac hypertrophy. Although impaired autophagic flux contributes to cardiac deterioration, the precise molecular mechanisms are still unclear. The ubiquitin-proteasome system serves as a critical regulator linking protein ubiquitination to autophagic flux and mitochondrial homeostasis. Asb2 (ankyrin repeat-containing protein with suppressor of cytokine signaling box 2), a muscle-specific E3 ubiquitin ligase essential for embryonic cardiogenesis, is uncharacterized in adult cardiac homeostasis and disease pathogenesis. Male mice with inducible cardiomyocyte-specific Asb2 knockout were generated to investigate Asb2's role in cardiac remodeling. Adeno-associated virus 9-mediated cardiomyocyte-specific Asb2 overexpression and KIF11 (kinesin family member 11) downregulation were used in transverse aortic constriction-induced hypertrophy and aging models. RNA sequencing, metabolite profiling, and mass spectrometry were used to assess the molecular mechanism by which Asb2 regulates cardiac metabolism and hypertrophy. Asb2β expression was significantly reduced in multiple forms of human cardiomyopathy and in hypertrophic murine hearts. Inducible Asb2 deletion in adult male mice led to the spontaneous development of cardiac hypertrophy and heart failure, accompanied by progressive accumulation of dysfunctional mitochondria and metabolic dysregulation. Mechanistically, Asb2 deficiency impaired ubiquitin-mediated degradation of KIF11, causing aberrant peripheral lysosomal redistribution and disrupting autophagosome-lysosome fusion, which resulted in impaired late-stage autophagic flux and metabolic disturbances. Notably, therapeutic restoration of Asb2 expression via adeno-associated virus 9-mediated delivery attenuated pressure overload-induced and age-related cardiac hypertrophy and heart failure. Moreover, both genetic and pharmacological inhibition of KIF11 effectively restored autophagic flux and mitochondrial homeostasis, thereby reversing pathological cardiac remodeling in Asb2-deficient hearts and transverse aortic constriction-induced cardiac dysfunction. Asb2 is a novel regulator of mitochondrial quality control in cardiomyocytes via KIF11-mediated lysosomal redistribution. Targeting the Asb2-KIF11 axis may be a promising strategy for improving mitochondrial homeostasis and cardiomyocyte function in chronic heart failure.
-
7. Acute Coronary Syndrome in Kawasaki Disease From Infancy to Adulthood.
PMID:日期:2026-09-22Acute coronary syndrome (ACS) remains underrecognized in patients with Kawasaki disease (KD). The population at risk for KD-associated ACS is increasing, yet current ACS guidelines are largely derived from atherosclerotic disease and do not adequately address the distinctive mechanisms, anatomy, and thrombosis risk associated with KD. Because the pathophysiology and management of KD-associated ACS differ in fundamental ways from those of atherosclerotic coronary artery disease, its management requires a coordinated team response, with collaboration between pediatric and adult cardiologists. Recent advances in coronary imaging, interventional techniques, and antithrombotic therapies provide an opportunity to establish a more disease-specific approach. This review synthesizes current evidence on the epidemiology and pathophysiology of coronary artery aneurysms, interventional coronary imaging, acute management, revascularization strategies, antithrombotic therapy, and post-ACS surveillance in patients with KD to guide clinical decision-making and treatment for patients with KD presenting with ACS.
-
10. The β-Blocker Breakup: Individualizing the AβYSS of Deprescription.
PMID:日期:2026-09-22该文献暂无摘要。