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| 1 | 2018 update of expert consensus statement on antiplatelet therapy in East Asian patients with ACS or undergoing PCI显示文摘East Asians are the most populous race in the world and their health status is an important global issue.Compared with Caucasian populations, East Asian patients have a different benefit/risk ratio when using antithrombotic treatment. Despite this observation, treatment strategies in East Asian patients are mostly based on the American and European guidelines. Despite a lower platelet inhibitory response to clopidogrel, East Asian patients show a similar or even a lower rate of ischemic event occurrence and higher bleeding risk compared with Caucasian patients. For potent P2Y_(12) inhibitors(ticagrelor and prasugrel),East Asian patients have shown less favorable net clinical benefits compared with Caucasian patients,which may be related to differences in pharmacokinetic/pharmacodynamic profiles and therapeutic zone of antiplatelet effect. This updated consensus mainly focuses on state-of-the-art and current controversies in the East Asian population. In addition, when East Asian patients are administered potent P2Y_(12) receptor inhibitors, the strategies and ongoing trials to overcome the related hurdles are discussed. | Yong Huo Young-Hoon Jeong Yanjun Gong Daowen Wang Ben He Jiyan Chen Guosheng Fu Yundai Chen Jianping Li Yi Li Shinya Goto Udaya S.Tantry Paul A.Gurbel Jong-Hwa Ahn Hyo-Soo Kim Myung Ho Jeong Yaling Han Sidney C.Smith Jr. Junbo Ge | 2019 | Science Bulletin2019，64，3： | 12 |
| 2 | Hydrogen sulfide suppresses transforming growth factor-β1-induced differentiation of human cardiac fibroblasts into myofibroblasts显示文摘In heart disease, transforming growth factor-β1(TGF-β1) converts fibroblasts into myofibroblasts, which synthesize and secrete fibrillar type I and III collagens. The purpose of the present study was to investigate how hydrogen sulfide(H2S) suppresses TGF-β1-induced differentiation of human cardiac fibroblasts to myofibroblasts. Human cardiac fibroblasts were serum-starved in fibroblast medium for 16 h before exposure to TGF-β1(10 ng m L-1) for 24 h with or without sodium hydrosulfide(Na HS, 100 μmol L-1, 30 min pretreatment) treatment. Na HS, an exogenous H2 S donor, potently inhibited the proliferation and migration of TGF-β1-induced human cardiac fibroblasts and regulated their cell cycle progression. Furthermore, Na HS treatment led to suppression of fibroblast differentiation into myofibroblasts, and reduced the levels of collagen, TGF-β1, and activated Smad3 in TGF-β1-induced human cardiac fibroblasts in vitro. We therefore conclude that H2 S suppresses TGF-β1-stimulated conversion of fibroblasts to myofibroblasts by inhibiting the TGF-β1/Smad3 signaling pathway, as well as by inhibiting the proliferation, migration, and cell cycle progression of human cardiac myofibroblasts. These effects of H2 S may play significant roles in cardiac remodeling associated with heart failure. | ZHANG YouEn WANG JiaNing LI Hua YUAN LiangJun WANG Lei WU Bing GE JunBo | 2015 | Science China(Life Sciences)2015，58，11： | 11 |
| 3 | Analysis of serum cardiac biomarkers and treadmill exercise test-electrocardiogram for the diagnosis of coronary heart disease in suspected patients显示文摘浆液蛋白质肌酸 kinase isoenzyme MB ( CK-MB )和心脏的 troponin T 是在临床的实践的心脏的 ischemic 损坏的经典 biomarkers ,它能易感知地检测心肌的坏死另外的二浆液蛋白质,修改局部缺血的白朊和N终端 pro-B-type natriuretic 肽( NT-proBNP ),最近作为心肌的局部缺血的新奇 biomarkers 被识别了。在这研究,四 biomarkers 在踏车锻练测试( TET )前后与怀疑的冠的心疾病( CHD )从 44 个合格病人在 sera 被检测,心电图( ECG )在 TET ( TET-ECG )和冠的 angiography ( CAG )的侵略检查期间被测量,它是 CHD 诊断的标准答案,也被执行。为 CAG, 25 个病人是积极的,, 19 为数字是的 TET-ECG 是否定的 19 和 25 分别地。在这四 biomarkers 之中,在 CAG 积极的组的 NT-proBNP 水平在 TET 前后两个都比在 CAG 否定的组的那些高得多,与在 TET 前的统计意义(P = 0.008 ) 。根据操作特征(巨鸟) 曲线的接收装置,而且,浆液 biomarker NT-proBNP 证明 CHD 和它的截止价值的诊断效果是 67 pg/ml,因此,在这的 30 个病人学习是积极的 NT-proBNP, 14 是否定的。并且是否独自或在里面与 TET-ECG 分析了联合,被发现 NT-proBNP 显然提高了考试的敏感。更重要地,在 NT-proBNP 和 TET-ECG 测试否定的所有病人结果是 CAG 否定,它意味着这二非侵略的考试的联合可能为 CHD 代替 CAG 的侵略检查诊断。与更多的病人一起的进一步的研究被保证在这份报纸验证调查结果。 | Zhenhua Zhu Yan Yan Qibing Wang Juying Qian Junbo Ge | 2010 | Acta Biochimica et Biophysica Sinica2010，42，1： | 10 |
| 4 | Exogenous taurine attenuates mitochondrial oxidative stress and endoplasmic reticulum stress in rat cardiomyocytes显示文摘公牛,有条件地必要的氨基酸,在心血管的功能起一个关键作用。这里,我们检验了效果在在老鼠 cardiomyocytes 的线粒体和 endoplasmic 蜂窝胃上公牛在葡萄糖剥夺(GD ) 期间。数据证明房间生存能力,细胞内部的公牛的内容,和公牛的 transporter 表示在 GD 期间被减少。相反,反应的氧种类的增加和细胞内部的 Ca2+ 内容被观察。也引起的 GD 破坏了展开的蛋白质反应(UPR ) 的 mitochondrial 膜潜力, apoptotic 房间死亡,和分离在 cardiomyocytes 的相对蛋白质。信号 transduction 分析证明那 Bcl-2 家庭蛋白质平衡被扰乱, caspase-12 被激活, UPR 亲戚蛋白质层次是起来调整的。而且,有 80 公里的预告的处理在 cardiomyocytes 的外长的公牛的稀释 GD 效果。我们的结果建议那公牛在禁止线粒体依赖者房间 apoptosis 和联系 UPR 的房间 apoptosis 上有有益的效果并且可能在未来在尖锐心肌的梗塞上有临床的含意。 | Yujie Yang Yue Zhang Xiaoyu Liu Ji Zuo Keqiang Wang Junbo Ge | 2013 | Acta Biochimica et Biophysica Sinica2013，45，5： | 10 |
| 5 | Active greeting technique: a mother-and-child catheter based technique to facilitate retrograde wire externalization in recanalization of coronary chronic total occlusion显示文摘Although retrograde approach has greatly improved the success rate of percutaneous coronary intervention(PCI) for coronary chronic total occlusion(CTO), retrograde wire externalization still remains challenging and time-consuming in some cases. Cases utilizing ‘‘Active Greeting Technique(AGT)', a mother-and-child catheter based technique to facilitate retrograde wire externalization, were extracted from Chronic Total Occlusion Club, China(CTOCC) database. AGT was performed by deep intubation a mother-and-child catheter(GuidezillaTMextension, 4 or 5 Fr inner catheter, and etc.) in combination with either reverse controlled antegrade or retrograde subintimal tracking(CART) technique or retrograde wire crossing technique. A total of 111 patients with 112 CTO lesions treated with this technique were retrospectively analyzed. Reverse CART technique and retrograde wire crossing technique were performed in 90.2% and 9.8% of all procedures. The utilization of GuidezillaTMextension, 4 Fr, and 5 Fr inner catheter accounted for 94.6%, 3.6%, and 1.8%, respectively. Externalization of retrograde wire was successful in all cases. No procedural complications were adjudicated to AGT. Complications independent of AGT included two target vessel perforations and two collateral perforations. No in-hospital major adverse cardiac events were found. AGT is a feasible and safe technique that facilitates retrograde wire externalization. | Junbo Ge Lei Ge Bin Zhang Xin Zhong Jianying Ma Leisheng Ru Tao Hu Juying Qian 无 | 2018 | Science Bulletin2018，63，23： | 10 |
| 6 | miR-210 over-expression enhances mesenchymal stem cell survival in an oxidative stress environment through antioxidation and c-Met pathway activation显示文摘microRNA-210(miR-210)has generally been reported to be associated with cell survival under hypoxia.However,there are few data regarding the role of miR-210 in the survival of mesenchymal stem cells(MSCs)under oxidative stress conditions.Thus,we sought to investigate whether miR-210 over-expression could protect MSCs against oxidative stress injury and what the primary mechanisms involved are.The results showed that over-expression of miR-210 significantly reduced the apoptosis of MSCs under oxidative stress,accompanied by obvious increases in cell viability and superoxide dismutase activity and remarkable decreases in malonaldehyde content and reactive oxygen species production,resulting in a noticeable reduction of apoptotic indices when compared with the control.Moreover,the above beneficial effects of miR-210 could be significantly reduced by c-Met pathway repression.Collectively,these results showed that miR-210 over-expression improved MSC survival under oxidative stress through antioxidation and c-Met pathway activation,indicating the potential development of a novel approach to enhance the efficacy of MSC-based therapy for injured myocardium. | XU JianFeng HUANG ZheYong LIN Li FU MingQiang GAO YanHua SHEN YunLi ZOU YunZeng SUN AiJun QIAN JuYing GE JunBo | 2014 | Science China(Life Sciences)2014，57，10： | 10 |
| 7 | Nine-month angiographic and two-year clinical follow-up of polymer-free sirolimus-eluting stent versus durable-polymer sirolimus-eluting stent for coronary artery disease: the Nano randomized trial显示文摘 | Zhang Yaojun Chen Fang Takashi Muramatsu Xu Bo Li Zhanquan Ge Junbo He Qing Yang Zhijian Li Shumei Wang Lefeng Wang Haichang He Ben Li Kang Qi Guoxian Li Tianchang Zeng Hesong Peng Jianjun Jiang Tieming Zeng Qiutang Zhu Jianhua Fu Guosheng Christos V. Bourantas Patrick W. Serruys Huo Yong | 2014 | Chinese Medical Journal2014，，11： | 8 |
| 8 | The critical roles of m6A modification in metabolic abnormality and cardiovascular diseases显示文摘N6-methyladenosine(m6A)RNA methylation is an emerging area of epigenetics,which is a reversible and dynamic modification mediating by‘writers’(methylase,adding methyl groups,METTL3,METTL14,and WTAP),‘erasers’(demethylase,deleting methyl groups,FTO and ALKBH5),and‘readers’(YTHDF1-3,YTHDC1 and YTHDC2).Recent studies in human,animal models and cell levels have disclosed a critical role of m6A modification in regulating the homeostasis of metabolic processes and cardiovascular function.Evidence from these studies identify m6A as a candidate of biomarker and therapeutic target for metabolic abnormality and cardiovascular diseases(CVD).Comprehensive understanding of the complexity of m6A regulation in metabolic diseases and CVD will be helpful for us to understand the pathogenesis of CVD.In this review,we discuss the regulatory role of m6A in metabolic abnormality and CVD.We will emphasize the clinical relevance of m6A dysregulation in CVD. | Beijian Zhang Hao Jiang Zhen Dong Aijun Sun Junbo Ge | 2021 | Genes & Diseases2021，8，6： | 8 |
| 9 | m6A demethylase FTO attenuates cardiac dysfunction by regulating glucose uptake and glycolysis in mice with pressure overload-induced heart failure显示文摘Dear Editor,N6-methyladenosine(m6A)is the most common posttranscriptional mammalian mRNA modification involved in multiple biological processes and diseases.1 However,its role in cardiac energy metabolism changes during heart failure(HF)remains elusive.Here we explored the role of m6A demethylase fat mass and obesity-associated protein(FTO)in glucose metabolism during pressure overload-induced HF.Methylated RNA immunoprecipitation sequencing(MeRIP-seq)was performed to map transcriptome-wide m6A modifications in transverse aortic constriction(TAC)and sham hearts.The number of identified m6A peaks was higher in the TAC than in the sham hearts(Fig.1a).Consistent with previous reports,the m6A peaks were enriched in 3’-untranslated regions in both the TAC and sham hearts(Fig.1b).2 The m6A peaks were characterized by the canonical RGAAR(R=A or G)motif(Fig.1c). | Beijian Zhang Hao Jiang Jian Wu Yun Cai Zhen Dong Yongchao Zhao Qinfeng Hu Kai Hu Aijun Sun Junbo Ge | 2021 | Signal Transduction and Targeted Therapy2021，6，12： | 6 |
| 10 | Alda-1 treatment promotes the therapeutic effect of mitochondrial transplantation for myocardial ischemia-reperfusion injury显示文摘Mitochondrial damage is a critical driver in myocardial ischemia-reperfusion(I/R)injury and can be alleviated via the mitochondrial transplantation.The efficiency of mitochondrial transplantation is determined by mitochondrial vitality.Because aldehyde dehydrogenase 2(ALDH2)has a key role in regulating mitochondrial homeostasis,we aimed to investigate its potential therapeutic effects on mitochondrial transplantation via the use of ALDH2 activator,Alda-1.Our present study demonstrated that time-dependent internalization of exogenous mitochondria by cardiomyocytes along with ATP production were significantly increased in response to mitochondrial transplantation.Furthermore,Alda-1 treatment remarkably promoted the oxygen consumption rate and baseline mechanical function of cardiomyocytes caused by mitochondrial transplantation.Mitochondrial transplantation inhibited cardiomyocyte apoptosis induced by the hypoxia-reoxygenation exposure,independent of Alda-1 treatment.However,promotion of the mechanical function of cardiomyocytes exposed to hypoxia-reoxygenation treatment was only observed after mitochondrial Alda-1 treatment and transplantation.By using a myocardial I/R mouse model,our results revealed that transplantation of Alda-1-treated mitochondria into mouse myocardial tissues limited the infarction size after I/R injury,which was at least in part due to increased mitochondrial potential-mediated fusion.In conclusion,ALDH2 activation in mitochondrial transplantation shows great potential for the treatment of myocardial I/R injury. | Xiaolei Sun Rifeng Gao Wenjia Li Yongchao Zhao Heng Yang Hang Chen Hao Jiang Zhen Dong Jingjing Hu Jin Liu Yunzeng Zou Aijun Sun Junbo Ge | 2021 | Bioactive Materials2021，6，7： | 5 |
| 11 | Limited value of recovery phase-limited ST segment depression of treadmill exercise test显示文摘 | Yang Hongbo Huang Zheyong Lou Yi Shen Yunli Qian Juying Ge Junbo | 2014 | Chinese Medical Journal2014，，4： | 3 |
| 12 | Assessment of Adaptive Rate Response Provided by Accelerometer, Minute Ventilation and Dual Sensor Compared with Normal Sinus Rhythm During Exercise: A Self-controlled Study in Chronotropically Competent Subjects显示文摘 | Yuanyuan Cao Yiqun Zhang Yangang Su Jin Bai Wei Wang Junbo Ge | 2015 | Chinese Medical Journal2015，，1： | 2 |
| 13 | Hepatitis B virus hijacks CTHRC1 to evade host immunity and maintain replication显示文摘HepatitisBvirus(HBV)infection causes acuteand chronic liver diseases,but is not directly cytopathic.Liver injury results fromrepeated attempts of the cellular immune response system to control the viral infection.Here,we investigate the roles of cellular factors and signaling pathways involved in the regulation of HBV replication to reveal the mechanism underlying HBV infection and pathogenesis.Weshowthat collagen triple helix repeat containing 1(CTHRC1)expression is elevated in HBV-infected patients andin HBV-transfected cells through epigenetic modification and transcriptional regulation.CTHRC1 facilitates HBV replication in cultured cells and BALB/c mice by activating the PKCa/ERK/JNK/c-Jun cascade to repress the IFN/JAK/STAT pathway.HBV-activated CTHRC1 downregulates the activityof typeI interferon(IFN),theproductionof IFN-stimulatedgenes(ISGs),andthephosphorylationofsignal transducerandactivator of transcription 1/2(STAT1/2),whereas it upregulates the phosphorylation and ubiquitination of type I IFN receptors(IFNARa/b).Thus,our results showthat HBV uses a novelmechanismto hijack cellular factors and signal cascades in order to evade host antiviral immunity and maintain persistent infection.We also demonstrate that CTHRC1 has a novel role in viral infection. | Lan Bai Wei Zhang Li Tan Hongchuan Yang Maolin Ge Chengliang Zhu Rui Zhang Yanhua Cao Junbo Chen Zhen Luo Wenzhe Ho Fang Liu Kailang Wu Jianguo Wu | 2015 | Journal of Molecular Cell Biology2015，7，6： | 2 |
| 14 | Comparision of intravascular ultrasound and angiography in the assessment of myocardial bridge显示文摘 | Junbo GE Raimund E Hans J | 1994 | Circulation1994，89，： | 1 |
| 15 | Characterization of chemical composition of Agaricus brasiliensis polysaccharides and its effect on myocardial SOD activity, MDA and caspase-3 level in ischemia–reperfusion rats显示文摘 | Song Zhang Ben He Junbo Ge Changlin Zhai Xin Liu Pingang Liu | 2010 | International Journal of Biological Macromolecules2010，，3： | 1 |
| 16 | Therapeutic silencing miR-146b-5p improves cardiac remodeling in a porcine model of myocardial infarction by modulating the wound reparative phenotype显示文摘Fibrotic remodeling is an adverse consequence of immune response-driven phenotypic modulation of cardiac cells following myocardial infarction(Ml).MicroRNA-146b(miR-146b)is an active regulator of immunomodulation,but its function in the cardiac inflammatory cascade and its clinical implication in fibrotic remodeling following Ml remain largely unknown.Herein,miR-146b-5p was found to be upregulated in the infarcted myocardium of mice and the serum of myocardial ischemia patients.Gain-and loss-of-function experiments demonstrated that miR-146b-5p was a hypoxia-induced regulator that governed the pro-fibrotic phenotype transition of cardiac cells.Overexpression of miR-146b-5p activated fibroblast proliferation,migration,and fibroblast-to-myofibroblast transition,impaired endothelial cell function and stress survival,and disturbed macrophage paracrine signaling.Interestingly,the opposite effects were observed when miR-146b-5p expression was inhibited.Luciferase assays and rescue studies demonstrated that the miR-146b-5p target genes mediating the above phenotypic modulations included interleukin 1 receptor associated kinase 1(IRAKI)and carcinoembryonic antigen related cell adhesion molecule 1(CEACAM1).Local delivery of a miR-146b-5p antagomir significantly reduced fibrosis and cell death,and upregulated capillary and reparative macrophages in the infarcted myocardium to restore cardiac remodeling and function in both mouse and porcine Ml models.Local inhibition of miR-146b-5p may represent a novel therapeutic approach to treat cardiac fibrotic remodeling and dysfunction following Ml. | Yiteng Liao Hao Li Hao Cao Yun Dong Lei Gao Zhongmin Liu Junbo Ge Hongming Zhu | 2021 | Protein & Cell2021，12，3： | 1 |
| 17 | High wall shear stress proximal to myocardial bridging and atherosclerosis:intracoronary ultrasound and pressure measurements显示文摘 | Ge Junbo Erbel R Gtsrge G | 1995 | Br Heart J1995，73，： | 1 |
| 18 | Red cell distribution width as a novel predictor of mortality in ICU patients显示文摘 | Feilong Wang Wenzhi Pan Shuming Pan Junbo Ge Shuyun Wang Miao Chen | 2011 | Annals of Medicine2011，，1： | 1 |
| 19 | Characterization of chemical composition of Agaricus brasiliensis polysaccharides and its effect on myocardial SOD activity, MDA and caspase-3 level in ischemia–reperfusion rats显示文摘 | Song Zhang Ben He Junbo Ge Changlin Zhai Xin Liu Pingang Liu | 2010 | International Journal of Biological Macromolecules2010，，3： | 1 |
| 20 | A novel mechanism for endothelial progenitor cells homing: The SDF-1/CXCR4–Rac pathway may regulate endothelial progenitor cells homing through cellular polarization显示文摘 | Li Shen Yongxing Gao Juying Qian Aijun Sun Junbo Ge | 2010 | Medical Hypotheses2010，，2： | 1 |
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