摘要：Molecular Medicine research-articleNo.12 P.e84–e100Protective Role of RNA Helicase DEAD-Box Protein 5 in Smooth Muscle Cell Proliferation and Vascular RemodelingRNA解旋酶DEAD-Box 蛋白5对平滑肌细胞增殖和血管重构的保护作用05-10 11:53 | 10.1161/CIRCRESAHA.119.314062。Methods and Results:The present study is a post hoc analysis of a prospective trial which randomized 696 ST-segment–elevation myocardial infarction patients with symptoms <12 hours 1:1:1 to either combined RIC and PostC in addition to primary PCI, PostC alone in addition to primary PCI, or conventional PCI (control). Three cycles of RIC were performed by inflation of an upper arm blood pressure cuff for 5 minutes followed by deflation for 5 minutes. PostC was performed after primary PCI via 4 cycles of 30 seconds balloon occlusions followed by 30 seconds of reperfusion. Major adverse cardiac events consisting of cardiac death, reinfarction, and new congestive heart failure were assessed during long-term follow-up. Follow-up data were obtained in 97% of patients in median 3.6 years after the index event (interquartile range, 2.9–4.2 years). Major adverse cardiac events occurred in 10.2% of patients in the combined RIC and PostC group and in 16.9% in the control group (odds ratio, 0.56。

TODAY

Pediatric CardiologyEarly Recent, May 09, 201901篇

Int J Cardiovasc ImagingEarly Recent, May 09, 201901篇

Der KardiologeEarly Recent, May 09, 201901篇

Herzschrittmacherther ElektrophysiolEarly Recent, May 09, 201901篇

Clin Res CardiolEarly Recent, May 09, 201901篇

Circulation ResearchMay 10, 2019: 124 (10)19篇

01

RNA解旋酶DEAD-Box 蛋白5对平滑肌细胞增殖和血管重构的保护作用

Ye Fan, Yikuan Chen, etc.

8小时前

Rationale:RNA helicases, highly conserved enzymes, are currently believed to be not only involved in RNA modulation, but also in other biological processes. We recently reported that RNA helicase DDX (DEAD-box protein)-5 is required for maintaining the homeostasis of vascular smooth muscle cells (SMCs). However, the expression and function of RNA helicase in vascular physiology and disease is unknown.

RNA螺旋酶是一种高度保守的酶，目前被认为不仅参与RNA调控，而且还参与其他生物学过程。我们最近报道，RNA解旋酶DDX（DEAD-Box蛋白）-5是维持血管平滑肌细胞（SMC）稳态所必需的。然而，RNA螺旋酶在血管生理学和疾病中的表达和功能尚不清楚。

Objective:To investigate the role of RNA helicase in vascular diseases.

探讨RNA解旋酶在血管疾病中的作用。

Methods and Results:We showed here that DDX-5 was the most abundant DEAD-box protein expressed in human and rodent artery, which mainly located in SMCs. It was demonstrated that DDX-5 levels were reduced in cytokine-stimulated SMCs and vascular lesions. DDX-5 knocking down or deficiency increased SMC proliferation and migration, whereas overexpression of DDX-5 prevented aberrant proliferation and migration of SMCs. Mechanistic studies revealed tranion factor GATA (GATA-binding protein)-6 as a novel downstream target of DDX-5, which directly interacted with GATA-6 and protected it from MDM (mouse double minute)-2–mediated degradation. Our ChIP assay identified a previously unreported binding of p27Kip1promoter to GATA-6. DDX-5 increased the recruitment of GATA-6 to p27Kip1promoter, which enhanced p27Kip1expression and maintained SMC quiescence. Finally, we showed exacerbated neointima formation in DDX-5 SMC-deficient mice after femoral artery injury, whereas overexpression of DDX-5 potently inhibited vascular remodeling in balloon-injured rat carotid artery.

我们发现，DDX-5是人类和啮齿动物动脉中表达最丰富的DEAD-Box蛋白，主要分布在SMC中。结果表明，细胞因子刺激的SMC和血管病变中DDX-5水平降低。DDX-5敲除或缺失可增加SMC的增殖和迁移，而DDX-5的过度表达可阻止SMC的异常增殖和迁移。机制研究显示转录因子GATA（GATA结合蛋白-6）是DDX-5的一个新的下游靶点，直接与GATA-6相互作用，保护其免受MDM（小鼠双分钟）介导的降解。我们的芯片分析确定了p27kip1启动子与GATA-6以前未报告的结合。DDX-5增加了GATA-6向p27kip1启动子的募集，从而增强p27kip1的表达并维持SMC的静止。最后，我们发现，在股动脉损伤后，DDX-5 SMC缺陷小鼠的新内膜形成加剧，而DDX-5的过度表达可有效抑制气球损伤大鼠颈动脉的血管重构。

Conclusions:These findings provide the first evidence for a role of RNA helicase DDX-5 in the protection against SMC proliferation, migration, and neointimal hyperplasia. Our data extend the fundamental role of RNA helicase beyond RNA modulation, which provides the basic information for new therapeutic strategies for vascular diseases.

这些发现为RNA解旋酶DDX-5在防止SMC增殖、迁移和新生内膜增生中的作用提供了第一个证据。我们的数据将RNA解旋酶的基本作用扩展到RNA调控之外，为血管疾病的新治疗策略提供了基础信息。

May 10, 2019: 124 (10), e84–e100

10.1161/CIRCRESAHA.119.314062

02

心肌透明质酸的合成与心肌巨噬细胞的反应密切相关，并促进缺血再灌注损伤后的愈合

Anne Petz, Maria Grandoch, etc.

8小时前

Rationale:Immediate changes in the ECM (extracellular matrix) microenvironment occur after myocardial ischemia and reperfusion (I/R) injury.

心肌缺血再灌注（I/R）损伤后，细胞外基质微环境会立即发生变化。

Objective:Aim of this study was to unravel the role of the early hyaluronan (HA)-rich ECM after I/R.

本研究旨在揭示I/R后早期富含透明质酸的ECM的作用。

Methods and Results:Genetic deletion ofHas2andHas1was used in a murine model of cardiac I/R. Chemical exchange saturation transfer imaging was adapted to image cardiac ECM post-I/R. Of note, the cardiac chemical exchange saturation transfer signal was severely suppressed byHas2deletion and pharmacological inhibition of HA synthesis 24 hours after I/R.Has2KO (Has2deficient) mice showed impaired hemodynamic function suggesting a protective role for endogenous HA synthesis. In contrast toHas2deficiency,Has1-deficient mice developed no specific phenotype compared with control post-I/R. Importantly, inHas2KO mice, cardiac macrophages were diminished after I/R as detected by19F MRI (magnetic resonance imaging) of perfluorcarbon-labeled immune cells, Mac-2/Galectin-3 immunostaining, and FACS (fluorescence-activated cell sorting) analysis (CD45CD11bLy6G−CD64F4/80cells). In contrast to macrophages, cardiac Ly6Chighand Ly6Clowmonocytes were unaffected post-I/R compared with control mice. Mechanistically, inhibition of HA synthesis led to increased macrophage apoptosis in vivo and in vitro. In addition, α-SMA (α-smooth muscle actin)–positive cells were reduced in the infarcted myocardium and in the border zone. In vitro, the myofibroblast response as measured byActa2mRNA expression was reduced by inhibition of HA synthesis and of CD44 signaling. Furthermore,Has2KO fibroblasts were less able to contract collagen gels in vitro. The effects of HA/CD44 on fibroblasts and macrophages post-I/R might also affect intercellular cross talk because cardiac fibroblasts were activated by monocyte/macrophages and, in turn, protected macrophages from apoptosis.

在小鼠心脏I/R模型中使用了Has2和Has1的基因缺失。化学交换饱和转移成像适用于I/R后的心脏ECM图像。值得注意的是，在I/R后24小时，HAS2缺失和药物抑制了HA合成，严重抑制了心脏化学交换饱和转移信号。（has2缺乏）小鼠的血流动力学功能受损，提示其对内源性HA合成具有保护作用。与has2缺乏相比，has1缺乏小鼠与对照组I/R后无特异性表型。重要的是，在has2 ko小鼠中，通过19f全氟碳标记免疫细胞的MRI（磁共振成像）、mac-2/galectin-3免疫染色和facs（荧光激活）检测到的I/R后，心肌巨噬细胞减少。细胞排序）分析（CD45 CD11B LY6G−CD64 F4/80 细胞）。与巨噬细胞相比，与对照小鼠相比，心脏Ly6Chrom和Ly6Chrom单核细胞在I/R后不受影响。从机制上讲，抑制HA合成导致体内和体外巨噬细胞凋亡增加。此外，在梗死心肌和交界区，α-SMA（α-平滑肌肌动蛋白）阳性细胞减少。在体外，通过抑制HA合成和CD44信号传导来降低由acta2 mRNA表达所测量的肌成纤维细胞反应。此外，HAS2-KO成纤维细胞在体外对胶原凝胶的收缩能力较差。HA/CD44对I/R后成纤维细胞和巨噬细胞的作用也可能影响细胞间的相互作用，因为心脏成纤维细胞被单核细胞/巨噬细胞激活，反过来又保护巨噬细胞免受凋亡。

Conclusions:Increased HA synthesis contributes to postinfarct healing by supporting macrophage survival and by promoting the myofibroblast response. Additionally, imaging of cardiac HA by chemical exchange saturation transfer post-I/R might have translational value.

增加的HA合成通过支持巨噬细胞存活和促进肌成纤维细胞反应促进梗死后愈合。另外，I/R术后化学交换饱和转移对心透明质酸的成像可能具有翻译价值。

May 10, 2019: 124 (10), 1433–1447

10.1161/CIRCRESAHA.118.313285

03

CRRL269

Yang Chen, Gail J. Harty, etc.

8小时前

Rationale:Acute kidney injury (AKI) has a high prevalence and mortality in critically ill patients. It is also a powerful risk factor for heart failure incidence driven by hemodynamic changes and neurohormonal activation. However, no drugs have been approved by the Food and Drug Administration. Endogenous pGC-A (particulate guanylyl cyclase A receptor) activators were reported to preserve renal function and improve mortality in AKI patients, although hypotension accompanied by pGC-A activators have limited their therapeutic potential.

急性肾损伤（AKI）在危重病人中具有很高的患病率和死亡率。它也是由血流动力学变化和神经激素激活引起的心力衰竭发病率的一个强有力的危险因素。但是，食品药品监督管理局没有批准任何药品。据报道，内源性PGC-A（颗粒性鸟苷酰环化酶A受体）活化剂可维持AKI患者的肾功能，提高死亡率，但同时伴有PGC-A活化剂的低血压限制了其治疗潜力。

Objective:We investigated the therapeutic potential of a nonhypotensive pGC-A activator/designer natriuretic peptide, CRRL269, in a short-term, large animal model of ischemia-induced AKI and also investigated the potential of uCNP (urinary C-type natriuretic peptide) as a biomarker for AKI.

我们研究了非低血压pgc-a激活剂/设计利钠肽（crrl269）在缺血诱导AKI的短期大动物模型中的治疗潜力，并研究了UCNP（尿c型利钠肽）作为AKI生物标记物的潜力。

Methods and Results:We first showed that CRRL269 stimulated cGMP generation, suppressed plasma angiotensin II, and reduced cardiac filling pressures without lowering blood pressure in the AKI canine model. We also demonstrated that CRRL269 preserved glomerular filtration rate, increased renal blood flow, and promoted diuresis and natriuresis. Further, CRRL269 reduced kidney injury and apoptosis as evidenced by ex vivo histology and tissue apoptosis analysis. We also showed, compared with native pGC-A activators, that CRRL269 is a more potent inhibitor of apoptosis in renal cells and induced less decreases in intracellular Ca2concentration in vascular smooth muscle cells. The renal antiapoptotic effects were at least mediated by cGMP/PKG pathway. Further, CRRL269 inhibited proapoptotic genes expression using a polymerase chain reaction gene array. Additionally, we demonstrated that AKI increased uCNP levels.

我们首先表明CRRL269刺激cGMP生成，抑制血浆血管紧张素II，并降低心脏充盈压力，而不降低AKI犬模型中的血压。我们还证明，CRRL269可维持肾小球滤过率，增加肾血流量，促进利尿和钠尿。此外，通过体外组织学和组织凋亡分析，CRRL269可减少肾损伤和凋亡。我们还发现，与天然PGC-A活化剂相比，CRRL269是一种更有效的肾细胞凋亡抑制剂，并诱导血管平滑肌细胞内Ca2 浓度降低。肾脏抗凋亡作用至少由cgmp/pkg途径介导。此外，使用聚合酶链反应基因阵列，CRRL269抑制凋亡前基因的表达。此外，我们证明AKI增加了UCNP水平。

Conclusions:Our study supports developing CRRL269 as a novel renocardiac protective agent for AKI treatment.

我们的研究支持将CRRL269作为一种新型的肾心保护剂用于AKI治疗。

May 10, 2019: 124 (10), 1462–1472

10.1161/CIRCRESAHA.118.314164

04

异细胞接触可支配动脉功能

Xiaohong Shu, Claire A. Ruddiman, etc.

8小时前

Rationale:Resistance arteries and conduit arteries rely on different relative contributions of endothelial-derived hyperpolarization versus nitric oxide to achieve dilatory heterocellular signaling. Anatomically, resistance arteries use myoendothelial junctions (MEJs), endothelial cell projections that make contact with smooth muscle cells. Conduit arteries have very few to no MEJs.

阻力动脉和导管动脉依赖内皮源性超极化与一氧化氮的不同相对作用来实现扩张性异细胞信号传导。在解剖学上，阻力动脉使用肌内皮连接（mejs），即与平滑肌细胞接触的内皮细胞投射。导管动脉很少甚至没有多发性硬化。

Objective:Determine if the presence of MEJs in conduit arteries can alter heterocellular signaling.

确定导管动脉中MEJS的存在是否能改变异细胞信号。

Methods and Results:We previously demonstrated that PAI-1 (plasminogen activator inhibitor-1) can regulate formation of MEJs. Thus, we applied pluronic gel containing PAI-1 directly to conduit arteries (carotid arteries) to determine if this could induce formation of MEJs. We found a significant increase in endothelial cell projections resembling MEJs that correlated with increased biocytin dye transfer from endothelial cells to smooth muscle cells. Next, we used pressure myography to investigate whether these structural changes were accompanied by a functional change in vasodilatory signaling. Interestingly, PAI-1-treated carotids underwent a switch from a conduit to resistance artery vasodilatory profile via diminished nitric oxide signaling and increased endothelial-derived hyperpolarization signaling in response to the endothelium-dependent agonists acetylcholine and NS309. After PAI-1 application, we also found a significant increase in carotid expression of endothelial alpha globin, a protein predominantly expressed in resistance arteries. Carotids from mice with PAI-1, but lacking alpha globin (Hba1−/−), demonstrated thatl-nitro-arginine methyl ester, an inhibitor of nitric oxide signaling, was able to prevent arterial relaxation.

我们以前证明PAI-1（纤溶酶原激活物抑制剂-1）可以调节MEJS的形成。因此，我们将含有PAI-1的普朗尼克凝胶直接应用于导管动脉（颈动脉），以确定这是否能够诱导MEJS的形成。我们发现内皮细胞投影显著增加，与内皮细胞向平滑肌细胞转移的生物胞浆染料增加相关。接下来，我们使用压力肌电图来研究这些结构变化是否伴随着血管舒张信号的功能变化。有趣的是，经PAI-1处理的类胡萝卜素通过减少一氧化氮信号和增加内皮源性超极化信号来响应内皮依赖性激动剂乙酰胆碱和NS309，从导管转变为阻力性动脉血管舒张。应用PAI-1后，我们还发现颈动脉内皮α-珠蛋白（一种主要在阻力动脉中表达的蛋白质）的表达显著增加。PAI-1小鼠的胡萝卜素缺乏α-珠蛋白（hba1−/−），这表明L-硝基精氨酸甲酯（一氧化氮信号的抑制剂）能够阻止动脉舒张。

Conclusions:The presence or absence of MEJs is an important determinant for influencing heterocellular communication in the arterial wall. In particular, alpha globin expression, induced within newly formed endothelial cell projections, may influence the balance between endothelial-derived hyperpolarization and nitric oxide–mediated vasodilation.

MEJS的存在与否是影响动脉壁细胞外通讯的重要决定因素。尤其是在新形成的内皮细胞投射中诱导的α-珠蛋白表达可能影响内皮源性超极化和一氧化氮介导的血管扩张之间的平衡。

May 10, 2019: 124 (10), 1473–1481

10.1161/CIRCRESAHA.118.313926

05

联合院内远隔缺血预处理和后处理改善ST段抬高型心肌梗死的临床疗效

Thomas Stiermaier, Jan-Oluf Jensen, etc.

8小时前

Rationale:Remote ischemic conditioning (RIC) or ischemic postconditioning (PostC) may protect the myocardium from ischemia-reperfusion injury in patients with ST-segment–elevation myocardial infarction.

远隔缺血预处理（RIC）或缺血后处理（PostC）可保护ST段抬高型心肌梗死患者心肌免受缺血再灌注损伤。

Objective:To determine whether combined intrahospital RIC and PostC or PostC alone in addition to primary percutaneous coronary intervention (PCI) reduce long-term clinical events after ST-segment–elevation myocardial infarction.

确定除了经皮冠状动脉介入治疗（PCI）外，合并院内RIC和PostC或单纯Post是否能减少ST段抬高型心肌梗死后的长期临床事件。

Methods and Results:The present study is a post hoc analysis of a prospective trial which randomized 696 ST-segment–elevation myocardial infarction patients with symptoms <12 hours 1:1:1 to either combined RIC and PostC in addition to primary PCI, PostC alone in addition to primary PCI, or conventional PCI (control). Three cycles of RIC were performed by inflation of an upper arm blood pressure cuff for 5 minutes followed by deflation for 5 minutes. PostC was performed after primary PCI via 4 cycles of 30 seconds balloon occlusions followed by 30 seconds of reperfusion. Major adverse cardiac events consisting of cardiac death, reinfarction, and new congestive heart failure were assessed during long-term follow-up. Follow-up data were obtained in 97% of patients in median 3.6 years after the index event (interquartile range, 2.9–4.2 years). Major adverse cardiac events occurred in 10.2% of patients in the combined RIC and PostC group and in 16.9% in the control group (odds ratio, 0.56; 95% CI, 0.32–0.97;P=0.04). The difference was driven by a significantly reduced rate of new congestive heart failure in the RIC and PostC group (2.7% versus 7.8%; odds ratio, 0.32; 95% CI, 0.13–0.84;P=0.02). In contrast, PostC alone did not reduce major adverse cardiac events compared with controls (14.1% versus 16.9%; odds ratio, 0.81; 95% CI, 0.48–1.35;P=0.41), and the reduction of new congestive heart failure was not statistically significant (3.5% versus 7.8%; odds ratio, 0.43; 95% CI, 0.18–1.03;P=0.05).

本研究是对一项前瞻性试验的事后分析，该试验将696例症状<12小时的ST段抬高型心肌梗死患者按1:1:1随机分为联合RIC与PostC的直接PCI组、单纯PostC的直接PCI组，以及常规PCI组（对照组）。用上臂血压袖带充气5分钟，然后放气5分钟，进行三次RIC循环。经4个周期的30秒球囊封堵术后，再灌注30秒进行直接PCI术后PostC。在长期随访中对主要不良心脏事件包括心脏死亡、再梗死和新发充血性心力衰竭进行了评估。在指标事件发生后3.6年的中位数中，97%的患者获得了随访数据（四分位间距，2.9-4.2年）。RIC和PostC联合治疗组中10.2%的患者发生严重心脏不良事件，对照组中16.9%的患者发生严重心脏不良事件（比值比0.56；95%可信区间0.32-0.97；P=0.04）。RIC组和Post组新发充血性心力衰竭的发生率显著降低（2.7% vs. 7.8%；比值比0.32；95%可信区间0.13-0.84；p=0.02），从而导致了这一差异。与对照组相比，单纯PostC并未减少主要不良心脏事件（14.1% vs. 16.9%；优势比，0.81；95%可信区间，0.48-1.35；p=0.41），并且新发充血性心力衰竭的减少没有统计学意义（3.5% vs. 7.8%；优势比，0.43；95%可信区间，0.18-1.03；p=0.05）。

Conclusions:Cardioprotection by combined intrahospital RIC and PostC in addition to primary PCI significantly reduced the rate of major adverse cardiac events and new congestive heart failure after ST-segment–elevation myocardial infarction.

在ST段抬高型心肌梗死后，直接PCI联合院内RIC和PostC进行心脏保护可显著降低主要不良心脏事件和新发充血性心力衰竭的发生率。

May 10, 2019: 124 (10), 1482–1491

10.1161/CIRCRESAHA.118.314500

CONTENTS

Pediatric CardiologyEarly Recent, May 09, 2019今日发布1篇文章

Case ReportNo.01 P.1-4Left Ventricular Pseudoaneurysm Following Surgical Repair of Ventricular Septal Defect in an Infant婴儿室间隔缺损修补术后左室假性动脉瘤05-09 21:14 | 10.1007/s00246-019-02119-x

Int J Cardiovasc ImagingEarly Recent, May 09, 2019今日发布1篇文章

Original PaperNo.01 P.1-11Hemodynamic impact of coronary stenosis using computed tomography: comparison between noninvasive fractional flow reserve and 3D fusion of coronary angiography with stress myocardial perfusionCT对冠状动脉狭窄血流动力学的影响：无创FFR与压力心肌灌注冠状动脉造影三维融合的比较05-09 21:38 | 10.1007/s10554-019-01618-5

Der KardiologeEarly Recent, May 09, 2019今日发布1篇文章

Journal ClubNo.01 P.1-2TAVI: je mehr Eingriffe, desto besser das Zentrum?TAVI: the more interventions, the better the center?干预：TAVI的越多越好的中心？干预：TAVI更多、更好的中心？05-09 21:49 | 10.1007/s12181-019-0325-2

Herzschrittmacherther ElektrophysiolEarly Recent, May 09, 2019今日发布1篇文章

SchwerpunktNo.01 P.1-6Fahreignung bei implantierten kardiovaskulären elektrischen GerätenFitness to drive in patients with cardiovascular implantable electronic devices心血管植入式电子设备患者的驾驶适应性05-09 22:43 | 10.1007/s00399-019-0626-y

Clin Res CardiolEarly Recent, May 09, 2019今日发布1篇文章

Letter to the EditorsNo.01 P.1-3Recurrent cardiac sarcoidosis after heart transplantation心脏移植后复发性心脏结节病05-09 22:52 | 10.1007/s00392-019-01485-z

Circulation ResearchMay 10, 2019: 124 (10)今日发布19篇文章

In This Issue in-briefNo.01 P.1401In This Issue本期推荐05-10 11:53 | 10.1161/RES.0000000000000274

Meet the First Authors in-briefNo.02 P.1402–1404Meet the First Authors认识第一批作者05-10 11:53 | 10.1161/RES.0000000000000273

Editorials editorialNo.03 P.1405–1407A DEAD-Box Stop of Vascular Remodeling血管重构的DEAD-box停止05-10 11:53 | 10.1161/CIRCRESAHA.119.315097

editorialNo.04 P.1408–1410Significance and Mechanistic Relevance of SIRT6-Mediated Endothelial Dysfunction in Cardiovascular Disease ProgressionSIRT6介导的内皮功能障碍在心血管疾病进展中的意义及机制相关性05-10 11:53 | 10.1161/CIRCRESAHA.119.315098

editorialNo.05 P.1411–1412I Kid(ney) You Not...Natriuretic Peptides Which Promote Natriuresis but Not Hypotension我跟你开玩笑，你不……利钠肽能促进钠中毒，但不会导致低血压05-10 11:53 | 10.1161/CIRCRESAHA.119.315129

Leaders in Cardiovascular Science research-articleNo.06 P.1413–1416David Lefer戴维莱弗05-10 11:53 | 10.1161/CIRCRESAHA.119.315207

research-articleNo.07 P.1417–1419Sean Wu吴昕05-10 11:53 | 10.1161/CIRCRESAHA.119.315208

News & Views newsNo.08 P.1420–1424Stanford Cardiovascular Institute斯坦福大学心血管研究所05-10 11:53 | 10.1161/CIRCRESAHA.119.310761

Viewpoints article-commentaryNo.09 P.1425–1427ApoB载脂蛋白B05-10 11:53 | 10.1161/CIRCRESAHA.119.315019

Beyond Science research-articleNo.10 P.1428–1429William Harvey and the Discovery of the Circulation of the Blood威廉·哈维和血液循环的发现05-10 11:53 | 10.1161/CIRCRESAHA.119.314978

research-articleNo.11 P.1430–1432Marcello Malpighi (1628–1694)马尔比基（1628–1694）05-10 11:53 | 10.1161/CIRCRESAHA.119.314936

Molecular Medicine research-articleNo.12 P.e84–e100Protective Role of RNA Helicase DEAD-Box Protein 5 in Smooth Muscle Cell Proliferation and Vascular RemodelingRNA解旋酶DEAD-Box 蛋白5对平滑肌细胞增殖和血管重构的保护作用05-10 11:53 | 10.1161/CIRCRESAHA.119.314062

research-articleNo.13 P.1433–1447Cardiac Hyaluronan Synthesis Is Critically Involved in the Cardiac Macrophage Response and Promotes Healing After Ischemia Reperfusion Injury心肌透明质酸的合成与心肌巨噬细胞的反应密切相关，并促进缺血再灌注损伤后的愈合05-10 11:53 | 10.1161/CIRCRESAHA.118.313285

Cellular Biology research-articleNo.14 P.1448–1461Endothelial SIRT6 Is Vital to Prevent Hypertension and Associated Cardiorenal Injury Through Targeting Nkx3.2-GATA5 Signaling内皮sirt6通过靶向NKX3.2-GATA5信号通路对预防高血压和相关的心肾损伤至关重要。05-10 11:53 | 10.1161/CIRCRESAHA.118.314032

Integrative Physiology research-articleNo.15 P.1462–1472CRRL269CRRL26905-10 11:53 | 10.1161/CIRCRESAHA.118.314164

research-articleNo.16 P.1473–1481Heterocellular Contact Can Dictate Arterial Function异细胞接触可支配动脉功能05-10 11:53 | 10.1161/CIRCRESAHA.118.313926

Clinical Track research-articleNo.17 P.1482–1491Combined Intrahospital Remote Ischemic Perconditioning and Postconditioning Improves Clinical Outcome in ST-Elevation Myocardial Infarction联合院内远隔缺血预处理和后处理改善ST段抬高型心肌梗死的临床疗效05-10 11:53 | 10.1161/CIRCRESAHA.118.314500

research-articleNo.18 P.1492–1504Prostate-Specific Antigen Within the Reference Range, Subclinical Coronary Atherosclerosis, and Cardiovascular Mortality参考范围内前列腺特异性抗原、亚临床冠状动脉粥样硬化和心血管死亡率05-10 11:53 | 10.1161/CIRCRESAHA.118.313413

Review review-articleNo.19 P.1505–1518HDL and Reverse Cholesterol Transport高密度脂蛋白和胆固醇的逆向转运05-10 11:53 | 10.1161/CIRCRESAHA.119.312617