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Exercise training attenuates angiotensinⅡ-induced cardiac fibrosis by reducing POU2F1 expression

Journal of Sport and Health science 2023年第4期12卷 464-476页

作者： Na Feng Haiyi Yu Yueshen Wang Youyi Zhang Han Xiao Wei Gao Department of Cardiology and Institute of Vascular Medicine Peking University Third HospitalNational Health Commission Key Laboratory of Cardiovascular Molecular Biology and Regulatory PeptidesKey Laboratory of Molecular Cardiovascular ScienceMinistry of EducationBeijing Key Laboratory of Cardiovascular Receptors ResearchBeijing 100191China Research Unit of Medical science Research Management/Basic and Clinical Research of Metabolic cardiovascular Diseases Chinese Academy of Medical SciencesBeijing 100191China

Background:Exercise training protects against heart failure.However,the mechanism underlying the protective effect of exercise training on angiotensinⅡ(AngⅡ)-induced cardiac fibrosis remains unclear.Methods:An exercise model involving C57BL/6N mice and 6 weeks of treadmill training was used.AngⅡ(1.44 mg/kg/day)was administered to induce cardiac fibrosis.RNA sequencing and bioinformatic analysis were used to identify the key factors mediating the effects of exercise training on cardiac fibrosis.Primary adult mouse cardiac fibroblasts(CFs)were used in vitro.Adeno-associated virus serotype 9 was used to overexpress POU domain,class 2,transcription factor 1(POU2F1)in vivo.Results:Exercise training attenuated AngⅡ-induced cardiac fibrosis and reversed 39 gene expression changes.The transcription factor regulating the largest number of these genes was POU2F1.Compared to controls,POU2F1 was shown to be signififcantly upregulated by AngⅡ,which is itself reduced by exercise training.In vivo,POU2F1 overexpression nullified the benefits of exercise training on cardiac fibrosis.In CFs,POU2F1 promoted cardiac fibrosis.CCAAT enhancer-binding proteinβ(C/EBPβ)was predicted to be the transcription factor of POU2F1and verified using a dual-luciferase reporter assay.In vivo,exercise training activated AMP-activated protein kinase(AMPK)and alleviated the increase in C/EBPβinduced by AngⅡ.In CFs,AMPK agonist inhibited the increase in C/EBPβand POU2F1 induced by Ang II,whereas AMPK inhibitor reversed this effect.Conclusion:Exercise training attenuates AngⅡ-induced cardiac fibrosis by reducing POU2F1.Exercise training inhibits POU2F1 by activating AMPK,which is followed by the downregulation of C/EBPβ,the transcription factor of POU2F1.

关键词： AMPK C/EBPβ Cardiac fibrosis Exercise POU2F1

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Autophagy mediates the secretion of macrophage migration inhibitory factor from cardiomyocytes upon serum-starvation

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science China(Life sciences) 2019年第8期62卷 1038-1046页

作者： Jimin Wu Xiangning Deng Juan Gao Wei Gao Han Xiao Xinyu Wang Youyi Zhang Department of Cardiology and Institute of Vascular Medicine Peking University Third HospitalNHC Key Laboratory of Cardiovascular Molecular Biology and Regulatory PeptidesKey Laboratory of Molecular Cardiovascular ScienceMinistry of EducationBeijing Key Laboratory of Cardiovascular Receptors Research

Macrophage migration inhibitory factor(MIF) is an inflammatory cytokine. It is elevated early in the blood of acute myocardial infarction patients. However, it is unclear whether and how MIF is released. This study investigated the cellular source and mechanism of MIF release from hearts. An ischemia-mimic treatment induced the secretion of MIF from neonatal rat cardiomyocytes but not from fibroblasts. The treatment did not cause significant leakage of lactate dehydrogenase, suggesting that ischemia induced the MIF secretion without causing severe cell damage. Plasma samples from patients with acute chest pain at the emergency department were collected for the detection of MIF. MIF levels in patients with acute coronary syndrome(ACS)increased early, when cardiac injury markers were not yet elevated, suggesting that ischemia can induce MIF secretion before the occurrence of severe myocardial damage. Serum-starvation caused MIF secretion from rat cardiomyocytes and Langendorffperfused rat hearts. The secretion was suppressed by the inhibition of autophagy by inhibitors or by silencing of Atg5. In conclusion, serum-starvation induces the secretion of MIF from cardiomyocytes via autophagy dependent pathway. Clarifying the mechanism of MIF secretion will be helpful for its application in the early diagnosis and treatment of ACS.

关键词： macrophage migration inhibitory factor cardiomyocyte ischemia autophagy secretion

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A case of applying left bundle branch pacing combined with atrioventricular node ablation to treat atrial fibrillation-induced heart failure

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Journal of Geriatric Cardiology 2021年第6期18卷 492-497页

作者： Lahati HA Li-Yun HE Lei LI Jiang-Li HAN Shu-Wang LIU Yuan ZHANG Wei XU Wei GAO Department of Cardiology and Institute of Vascular Medicine Peking University Third HospitalNHC Key Laboratory of Cardiovascular Molecular Biology and Regulatory PeptidesKey Laboratory of Molecular Cardiovascular ScienceMinistry of EducationBeijing Key Laboratory of Cardiovascular Receptors ResearchBeijingChina

The core treatment of rapid arrhythmiainduced heart failure(HF)is to control the ventricular rate to an optimized lower level,which is usually achieved with various anti-arrhythmic drugs.However,arrhythmias may not respond well to pharmaceutical treatment for various reasons.Iatrogenic atrioventricular(AV)node ablation needs to be performed under these extreme conditions to lower the patient’s heart rate.

关键词： drugs fibrillation ventricular

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AMPK and cardiac remodelling

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science China(Life sciences) 2018年第1期61卷 14-23页

作者： Yenan Feng Youyi Zhang Han Xiao Department of Cardiology and Institute of Vascular Medicine Peking University Third Hospital Key Laboratory of Cardiovascular Molecular Biology and Regulatory Peptides Ministry of Health Key Laboratory of Molecular Cardiovascular Science Ministry of Education Beijing Key Laboratory of Cardiovascular Receptors Research

Cardiac remodelling is generally accepted as a critical process in the progression of heart failure. Myocyte hypertrophy,inflammatory responses and cardiac fibrosis are the main pathological changes associated with cardiac remodelling.AMP-activated protein kinase(AMPK) is known as an energy sensor and a regulator of cardiac metabolism under normal and ischaemic conditions. Additionally, AMPK has been shown to play roles in cardiac remodelling extending well beyond metabolic regulation. In this review, we discuss the currently defined roles of AMPK in cardiac remodelling and summarize the effects of AMPK on cardiac hypertrophy, inflammatory responses and fibrosis and the molecular mechanisms underlying these effects. In addition, we discuss some pharmacological activators of AMPK that are promising treatments for cardiac remodelling.

关键词： AMPK 心脏新陈代谢力传感器蛋白质病理学管理者药理学

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Cardiac Hypertrophy is Positively Regulated by MicroRNA-24 in Rats

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Chinese Medical Journal 2018年第11期131卷 1333-1341页

作者： Juan Gao Min Zhu Rui-Feng Liu Jian-Shu Zhang Ming Xu Department of Cardiology and Institute of Vascular Medicine Peking University Third Hospital key laboratory of cardiovascular molecular Biology and Regulatory Peptides Ministry of Health Key Laboratory of Molecular Cardiovascular Science Ministry of Education Beijing key laboratory of cardiovascular Receptors Research Beijing 100191 China

Background： MicroRNA-24 （miR-24） plays an important role in heart failure by reducing the efficiency of myocardial excitation-contraction coupling. Prolonged cardiac hypertrophy may lead to heart failure, but little is known about the role of miR-24 in cardiac hypertrophy. This study aimed to preliminarily investigate the function of miR-24 and its mechanisms in cardiac hypertrophy. Methods： Twelve Sprague-Dawley rats with a body weight of 50 ± 5 g were recruited and randonlly divided into two groups： a transverse aortic constriction （TAC） group and a sham surgery group. Hypertrophy index was measured and calculated by echocardiography and hematoxylin and eosin staining. TargetScans algorithm-based prediction was used to search for the targets of miR-24, which was subsequently confirmed by a real-time polymerase chain reaction and luciferase assay, lmmunofluorescence labeling was used to measure the cell surface area, and 3H-leucine incorporation was used to detect the synthesis of total protein in neonatal rat cardiac myocytes （NRCMs） with the overexpression of miR-24. In addition, flow cytometry was performed to observe the alteration in the cell cycle. Statistical analysis was carried out with GraphPad Prism v5.0 and SPSS 19.0. A two-sided P 〈 0.05 was considered as the threshold for significance. Results： The expression of miR-24 was abnormally increased in TAC rat cardiac tissue （ t =-2.938, P 〈 0.05）. TargetScans algorithm-based prediction demonstrated that CDKN 1B （p27, Kip 1 ）, a cell cycle regulator, was a putative target of miR-24, and was confirmed by luci ferase assay. The expression of p27 was decreased in TAC rat cardiac tissue （t = 2.896, P 〈 0.05）. The overexpression of miR-24 in NRCMs led to the decreased expression of p27 （t = 4.400, P 〈 0.01 ）, and decreased G0/G 1 arrest in cell cycle and cardiomyocylc hypertrophy. Conclusion： MiR-24 promotes cardiac hypertrophy partly by affecting the cell cycle through down-regulation of p27 expression.

关键词： Cardiac Hypertrophy Cell Cycle MicroRNA MicroRNA-24 p27

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Metabolic disorder in the progression of heart failure

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science China(Life sciences) 2019年第9期62卷 1153-1167页

作者： Xiuxiu Zhang Huiying Liu Juan Gao Min Zhu Yupeng Wang Changtao Jiang Ming Xu Department of Cardiology and Institute of Vascular Medicine Peking University Third Hospital/ NHC Key Laboratory of Cardiovascular Molecular Biology and Regulatory PeptidesKey Laboratory of Molecular Cardiovascular ScienceMinistry of EducationBeijing Key Laboratory of Cardiovascular Receptors ResearchBeijing 100191China Department of Physiology and Pathophysiology School of Basic Medical SciencesPeking UniversityKey Laboratory of Molecular Cardiovascular ScienceMinistry of Education and Beijing Key Laboratory of Cardiovascular Receptors ResearchBeijing 100191China State key laboratory of Natural and Biomimetic Drugs School of Pharmaceutical SciencesPeking UniversityBeijing 100191China

Heart failure(HF) is a major clinical concern owing to its high prevalence and high mortality.Metabolomics,an effective approach to predict diagnostic biomarkers and to explore the altered metabolic pathways in pathogenesis,has been extensively applied in evaluating the course of diseases.In this study,we used this approach to analyse the abundance of metabolites,with liquid chromatograph-mass spectrometer,in plasma samples from rats with transverse aortic constriction(TAC) and patients at different stages of HF.We compared the metabolic parameters within and between TAC rats and patients.An apparent metabolic shift was observed in rats,from compensated hypertrophy stage to decompensated hypertrophy stage,and in patients with HF,from stage A to stage B and subsequently stage C.Diagnostic biomarkers were predicted by comparing the variable importance in the projection scores and fold change analysis within and between rats and patients.Enrichment pathway analysis and network analysis provided an overview of the largely disturbed metabolic pathways,and those interfered at different stages and across species were confirmed.The significantly changed metabolites and pathways revealed the underlying mechanisms of HF pathogenesis,hinted at novel potential biomarkers,and provided potential therapeutic intervention targets for HF.

关键词： heart failure metabolomics TAC HF stages A–C biomarker pathway analysis

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A time sequential microfluid sensor with Tesla valve channels

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Nano Research 2023年第9期16卷 11667-11673页

作者： Pengcheng Zhao Haobin Wang Yaozheng Wang Wei Zhao Mengdi Han Haixia Zhang National key laboratory of science and Technology on Micro/Nano Fabrication Beijing Advanced Innovation Center for Integrated CircuitsSchool of Integrated CircuitsPeking UniversityBeijing 100871China Department of Cardiology and Institute of Vascular Medicine NHC Key Laboratory of Cardiovascular Molecular Biology and Regulatory PeptidesKey Laboratory of Molecular Cardiovascular ScienceMinistry of EducationBeijing Key Laboratory of Cardiovascular Receptors ResearchPeking University Third HospitalBeijing 100191China Department of Biomedical Engineering College of Future Technology Peking UniversityBeijing 100871China

The concentration of biomarkers in sweat can be used to evaluate human health,making efficient sweat sensing a focus of research.While flow channel design is often used to detect sweat velocity,it is rarely incorporated into the sensing of biomarkers,limiting the richness of sensing results.In this study,we report a time sequential sensing scheme for uric acid in sweat through a sequential design of Tesla valve channels.Graphene electrodes for detecting uric acid and directional Tesla valve flow channels were fabricated using laser engraving technology to realize time sequential sensing.The performance of the channels was verified through simulation.The time sequential detection of uric acid concentration in sweat can help researchers improve the establishment of human health management systems through flexible wearable devices.

关键词： time sequential sensing uric acid Tesla valves laser engraving technology

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Pathological matrix stiffness promotes cardiac fibroblast differentiation through the POU2F1 signaling pathway

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science China(Life sciences) 2021年第2期64卷 242-254页

作者： Mingzhe Li Jimin Wu Guomin Hu Yao Song Jing Shen Junzhou Xin Zijian Li Wei Liu Erdan Dong Ming Xu Youyi Zhang Han Xiao Department of Cardiology and Institute of Vascular Medicine Peking University Third Hospital/NHC Key Laboratory of Cardiovascular Molecular Biology and Regulatory Peptides/Key Laboratory of Molecular Cardiovascular ScienceMinistry of Education/Beijing Key Laboratory of Cardiovascular Receptors ResearchBeijing 100191China Division of cardiovascular sciences Faculty of Biology Medicine and HealthUniversity of ManchesterManchester M139PTUK Institute of cardiovascular sciences Health Science CenterPeking UniversityBeijing 100191China

Cardiac fibroblast(CF)differentiation into myofibroblasts is a crucial cause of cardiac fibrosis,which increases in the extracellular matrix(ECM)stiffness.The increased stiffness further promotes CF differentiation and fibrosis.However,the molecular mechanism is still unclear.We used bioinformatics analysis to find new candidates that regulate the genes involved in stiffnessinduced CF differentiation,and found that there were binding sites for the POU-domain transcription factor,POU2F1(also known as Oct-1),in the promoters of 50 differentially expressed genes(DEGs)in CFs on the stiffer substrate.Immunofluorescent staining and Western blotting revealed that pathological stiffness upregulated POU2F1 expression and increased CF differentiation on polyacrylamide hydrogel substrates and in mouse myocardial infarction tissue.A chromatin immunoprecipitation assay showed that POU2F1 bound to the promoters of fibrosis repressors IL1R2,CD69,and TGIF2.The expression of these fibrosis repressors was inhibited on pathological substrate stiffness.Knockdown of POU2F1 upregulated these repressors and attenuated CF differentiation on pathological substrate stiffness(35 kPa).Whereas,overexpression of POU2F1 downregulated these repressors and enhanced CF differentiation.In conclusion,pathological stiffness upregulates the transcription factor POU2F1 to promote CF differentiation by inhibiting fibrosis repressors.Our work elucidated the crosstalk between CF differentiation and the ECM and provided a potential target for cardiac fibrosis treatment.

关键词： fibroblast differentiation matrix stiffness POU2F1 cardiac fibrosis transcription factor

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Recurrent vital thrombotic events in a young man with FVIII gene duplication

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Chinese Medical Journal 2021年第8期134卷 996-998页

作者： Ling-Li Wang Dan Liu Na Feng Mu-Ye Ping Jiang-Li Han Wei Gao Fang-Fang Wang Department of Cardiology and Institute of Vascular Medicine Peking University Third HospitalNHC Key Laboratory of Cardiovascular Molecular Biology and Regulatory PeptidesKey Laboratory of Molecular Cardiovascular ScienceMinistry of EducationBeijing Key Laboratory of Cardiovascular Receptors ResearchBeijing 100191China Department of laboratory Medicine Peking University Third HospitalBeijing 100191China

To the Editor:The coagulation system is a complex regulatory system in the human body.In this case,the young patient had various vital thrombosis,including cerebral venous sinus thrombosis(CVST),coronary thrombosis,and left ventricular thrombus.However,the patient had neither hypercoagulable-related diseases nor risks nor coagulative or fibrinolytic protein deficiency.[1] Further genetic testing did not show the usual gene mutations relevant to coagulation dysfunction.W e report such a patient with a slight elevation in coagulation FVIII activity and a rare FVIII gene duplication.

关键词： diseases cerebral coronary

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The mechanism and therapy of aortic aneurysms

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Signal Transduction and Targeted Therapy 2023年第3期8卷 963-982页

作者： Jianing Gao Huanhuan Cao Gaofei Hu Yufei Wu Yangkai Xu Hongtu Cui Hong S.Lu Lemin Zheng The Institute of cardiovascular sciences and Institute of Systems Biomedicine School of Basic Medical SciencesKey Laboratory of Molecular Cardiovascular Science of Ministry of EducationNHC Key Laboratory of Cardiovascular Molecular Biology and Regulatory PeptidesBeijing Key Laboratory of Cardiovascular Receptors ResearchHealth Science CenterPeking University100191 BeijingChina Department of Cardiology and Institute of Vascular Medicine Peking University Third HospitalNHC Key Laboratory of Cardiovascular Molecular Biology and Regulatory PeptidesKey Laboratory of Molecular Cardiovascular ScienceMinistry of EducationBeijing Key Laboratory of Cardiovascular Receptors ResearchResearch Unit of Medical Science Research Management/Basic and Clinical Research of Metabolic Cardiovascular DiseasesChinese Academy of Medical Sciences100191 BeijingChina Department of Physiology Saha Cardiovascular Research CenterUniversity of KentuckySouth LimestoneLexingtonKY 40536-0298USA

Aortic aneurysm is a chronic aortic disease affected by many factors.Although it is generally asymptomatic,it poses a significant threat to human life due to a high risk of rupture.Because of its strong concealment,it is difficult to diagnose the disease in the early stage.At present,there are no effective drugs for the treatment of aneurysms.Surgical intervention and endovascular treatment are the only therapies.Although current studies have discovered that inflammatory responses as well as the production and activation of various proteases promote aortic aneurysm,the specific mechanisms remain unclear.Researchers are further exploring the pathogenesis of aneurysms to find new targets for diagnosis and treatment.To better understand aortic aneurysm,this review elaborates on the discovery history of aortic aneurysm,main classification and clinical manifestations,related molecular mechanisms,clinical cohort studies and animal models,with the ultimate goal of providing insights into the treatment of this devastating disease.The underlying problem with aneurysm disease is weakening of the aortic wall,leading to progressive dilation.If not treated in time,the aortic aneurysm eventually ruptures.An aortic aneurysm is a local enlargement of an artery caused by a weakening of the aortic wall.The disease is usually asymptomatic but leads to high mortality due to the risk of artery rupture.

关键词： aortic diagnosis drugs treatment

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