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Arterial thrombosis in the context of HCV-associated vascular disease can be prevented by protein C

Cellular & Molecular Immunology 2017年第12期14卷 986-996页

作者： Philipp Blüm Joachim Pircher Monika Merkle Thomas Czermak Andrea Ribeiro Hanna Mannell Florian Krötz Alexander Hennrich Michael Spannagl Simone Köppel Erik Gaitzsch Markus Wörnle Medizinische Klinik und Poliklinik IV InnenstadtKlinikum der Universität München80336 MünchenGermany walter brendel centre of experimental medicine and munich heart alliance Ludwig Maximilians University München80336 MünchenGermany Medizinische Klinik und Poliklinik I Klinikum der Universität München80336 MünchenGermany Abteilung für Transfusionsmedizin Zelltherapeutika und HämostaseologieKlinikum der Universität München80336 MünchenGermany

Hepatitis C virus(HCV)infection is a major problem *** is not limited to liver disease but is frequently complicated by immune-mediated extrahepatic manifestations such as glomerulonephritis or vasculitis.A fatal complication of HCV-associated vascular disease is ***:polyribocytidylic acid(poly(I:C)),a synthetic analog of viral RNA,induces a Toll-like receptor 3(TLR3)-dependent arteriolar thrombosis without significant thrombus formation in venules in *** procoagulant effects are caused by increased endothelial synthesis of tissue factor and PAI-1 without platelet *** addition to human umbilical endothelial cells(HUVEC),human mesangial cells(HMC)produce procoagulatory factors,cytokines and adhesion molecules after stimulation with poly(I:C)or HCV-containing cryoprecipitates from a patient with a HCV infection as *** protein C(APC)is able to prevent the induction of procoagulatory factors in HUVEC and HMC in vitro and blocks the effects of poly(I:C)and HCV-RNA on the expression of cytokines and adhesion molecules in HMC but not in *** vivo,protein C inhibits poly(I:C)-induced arteriolar ***,endothelial cells are de facto able to actively participate in immune-mediated vascular thrombosis caused by viral ***,we provide evidence for the ability of protein C to inhibit TLR3-mediated arteriolar thrombosis caused by HCV infection.

关键词： hepatitis C thrombosis toll-like receptor 3

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Animal models of pulmonary hypertension due to left heart disease

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Animal Models and experimental medicine 2022年第3期5卷 197-206页

作者： Shao-Fei Liu Yi Yan Charité-Universitätsmedizin Berlin Corporate Member of Freie Universität BerlinHumboldt-Universität zu Berlinand Berlin Institute of HealthBerlinGermany DZHK(German centre for Cardiovascular Research) Partner Site BerlinBerlinGermany Institute for Cardiovascular Prevention(IPEK) Ludwig-Maximilians-University MunichMunichGermany DZHK(German centre for Cardiovascular Research) Partner Site Munich Heart AllianceMunichGermany

Pulmonary hypertension due to left heart disease(PH-LHD) is regarded as the most prevalent form of pulmonary hypertension(PH). Indeed, PH is an independent risk factor and predicts adverse prognosis for patients with left heart disease(LHD). Clinically, there are no drugs or treatments that directly address PH-LHD, and treatment of LHD alone will not also ameliorate PH. To target the underlying physiopathological alterations of PH-LHD and to develop novel therapeutic approaches for this population, animal models that simulate the pathophysiology of PH-LHD are required. There are several available models for PH-LHD that have been successfully employed in rodents or large animals by artificially provoking an elevated pressure load on the left heart, which by transduction elicits an escalated pressure in pulmonary artery. In addition, metabolic derangement combined with aortic banding or vascular endothelial growth factor receptor antagonist is also currently applied to reproduce the phenotype of PH-LHD. As of today, none of the animal models exactly recapitulates the condition of patients with PH-LHD. Nevertheless, the selection of an appropriate animal model is essential in basic and translational studies of PH-LHD. Therefore, this review will summarize the characteristics of each PH-LHD animal model and discuss the advantages and limitations of the different models.

关键词： animal model l eft ventricular failure metabolic syndrome pulmonary hypertension due to left heart disease pulmonary vascular remodeling

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Implication of proliferation gene biomarkers in pulmonary hypertension

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Animal Models and experimental medicine 2021年第4期4卷 369-380页

作者： Yi Yan Rong Jiang Ping Yuan Li Wen Xiao-Bin Pang Zhi-Cheng Jing Yang-Yang He Zhi-Yan Han Institute for Cardiovascular Prevention(IPEK) Ludwig-Maximilians-University MunichMunichGermany DZHK(German centre for Cardiovascular Research) partner site Munich Heart AllianceMunichGermany Department of Cardio-Pulmonary Circulation Shanghai Pulmonary HospitalTongji University School of MedicineShanghaiChina Department of Cardiology The First Affiliated HospitalChongqing Medical UniversityChongqingChina School of Pharmacy Henan UniversityHenanChina State Key Laboratory of Complex Severeand Rare Diseasesand Department of CardiologyPeking Union Medical College HospitalChinese Academy of Medical Sciences and Peking Union Medical CollegeBeijingChina State Key Laboratory of Cardiovascular Disease and FuWai Hospital Chinese Academy of Medical Sciences and Peking Union Medical CollegeBeijingChina

Objective/Background:Proliferation is a widely recognized trigger for pulmonary hypertension(PH),a life-threatening,progressive disorder of pulmonary blood *** study was aimed to identify some proliferation associated genes/targets for better comprehension of PH ***:Human pulmonary arterial smooth muscle cells(hPASMCs)were cultured in the presence or absence of human recombinant platelet derived growth factor(rhPDGF)-*** were collected for metabolomics or transcriptomics *** profiling of lungs of PH rats after hypoxia exposure or of PH patients were retrieved from GEO ***:90 metabolites(VIP score>1,fold change>2 or2 or<0.5 and p<.05).152 differentially expressed MAGs were then determined,out of which 9 hub genes(IL6,CXCL8,CCL2,CXCR4,CCND1,PLAUR,PLAU,HBEGF and F3)were defined as core proliferation associated hub genes in protein proten interaction *** addition,the hub gene-based LASSO model can predict the occurrence of PH(AUC=0.88).The expression of CXCR4,as one of the hub genes,was positively correlated to immune cell ***:Our findings revealed some key proliferation associated genes in PH,which provide the crucial information concerning complex metabolic reprogramming and inflammatory modulation in response to proliferation signals and might offer therapeutic gains for PH.

关键词： metabolism associated genes metabolomics proliferation pulmonary hypertension transcriptomics

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Aging impairs the neurovascular interface in the heart

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四川生理科学杂志 2023年第9期45卷 1661-1661页

作者： Julian U G Wagner Institute of Cardiovascular Regeneration Centre for Molecular Medicine Goethe University Frankfurt 60590 Frankfurt Germany. German Center for Cardiovascular Research (DZHK) Partner Site Rhein-Main 60590 Frankfurt Germany. Cardiopulmonary Institute (CPI) 60590 Frankfurt Germany. Institute for Cardiovascular Physiology Goethe University Frankfurt 60590 Frankfurt Germany. Institute for Cardiovascular Prevention Ludwig-Maximilians-Universität München (LMU) 80336 Munich Germany. munich Cluster for Systems Neurology (SyNergy) 81377 Munich Germany. German Center for Cardiovascular Research (DZHK) Partner Site Munich Munich Heart Alliance (MHA) 80802 Munich Germany. Department of Biochemistry Cardiovascular Research Institute Maastricht (CARIM) Maastricht University Maastricht Netherlands. Department of Cardiology Pulmonology and Vascular Medicine Medical Faculty Heinrich-Heine-University Düsseldorf 40225 Düsseldorf Germany. Institute of Neural and Sensory Physiology Medical Faculty and University Hospital Düsseldorf Heinrich-Heine-University Düsseldorf 40225 Düsseldorf Germany. Division of Cardiology/Angiology/Intensive Care EVK Düsseldorf cNEP cardiac Neuro- and Electrophysiology Research Consortium 40217 Düsseldorf Germany. Cardiovascular Research Institute Düsseldorf (CARID) Medical Faculty and University Hospital of Düsseldorf Heinrich-Heine University Düsseldorf 40225 Düsseldorf Germany. Department of medicine I University Hospital Munich Ludwig Maximilian University 81377 Munich Germany. Institute of Surgical Research at the walter-brendel-centre of experimental medicine University Hospital LMU Munich 81377 Munich Germany. Interfaculty Center for Endocrine and Cardiovascular Disease Network Modelling and Clinical Transfer (ICON) LMU Munich 80539 Munich Germany. Max Planck Institute for heart and Lung Research 61231 Bad Nauheim Germany. Institute of Molecular and Translational Therapeutic Strategies (IMTTS) Hannover Medical School 30625 Hannover Germany. RE

Aging is a major risk factor for impaired cardiovascular *** the aging myocardium is characterized by microcirculatory dysfunction,and because nerves align with vessels,we assessed the impact of aging on the cardiac neurovascular *** report that aging reduces nerve density in the ventricle and dysregulates vascular-derived neuroregulatory *** down-regulates microRNA 145(miR-145)and derepresses the neurorepulsive factor ***-145 deletion,which increased Sema3a expression or endothelial Sema3a overexpression,reduced axon density,mimicking the aged-heart *** of senescent cells,which accumulated with chronological age in parallel to the decline in nerve density,rescued age-induced denervation,reversed Sema3a expression,preserved heart rate patterns,and reduced electrical *** data suggest that senescence-mediated regulation of nerve density contributes to age-associated cardiac dysfunction.

关键词： reversed aging interface

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Subcutaneous or Transvenous Defibrillator Therapy

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四川生理科学杂志 2021年第1期43卷 125-125页

作者： Reinoud E Knops From the heart Center Department of Clinical and Experimental Cardiology Amsterdam Cardiovascular Sciences Amsterdam University Medical Centers University of Amsterdam (R.E.K. L.R.A.O.N. L.V.A.B. T.F.B. A.-F.B.E.Q. L.S. W.S. A.W. K.C.W. J.R.G. K.M.K. M.C.B. J.G.P.T. A.A.M.W.) ERN GUARD-Heart (E.R.B. P.D.L. A.A.M.W.) and the Department of Cardiology OLVG (J.S.S.G.J.) Amsterdam the Department of Cardiology Isala Heart Centre Zwolle (P.-P.H.M.D.) the Department of Cardiology St. Antonius Hospital Nieuwegein (L.V.A.B.) the Department of Cardiology Flevoziekenhuis Almere (N.R.B.) the Department of Cardiology Radboud University Medical Center Nijmegen (M.A.B.) the Department of Cardiology Cardiovascular Research Institute Maastricht Maastricht University Medical Center Maastricht (K.V.) the Department of Cardiology Amphia Hospital Breda (M.A.) Werkgroep Cardiologische Centra Nederland Utrecht (M.A.) and the Department of Electrophysiology Catharina Hospital Eindhoven (F.A.L.E.B.) - all in the Netherlands the First Department of medicine-Cardiology University Medical Center Mannheim and the German Center for Cardiovascular Research Partner Site Heidelberg-Mannheim Mannheim (J.K.) Klinik für Innere Medizin III Schwerpunkt Kardiologie und Angiologie Universitätsklinikum Schleswig-Holstein Campus Kiel Kiel (H.B.) the Department of Medicine I Ludwig-Maximilians University Hospital and the German Center for Cardiovascular Research Munich Heart Alliance Munich (S.K.) and the Department of Electrophysiology Heart Center at University of Leipzig Leipzig (S.R.) - all in Germany the Division of Cardiology Section of Electrophysiology Emory University Atlanta (M.F.E.-C.) the Cardiology Clinical Academic Group St. George's University of London and St. George's University Hospitals NHS Foundation Trust London (E.R.B.) and Office of the Director of Clinical Electrophysiology Research and Lead for Inherited Arrhythmia Specialist Services University College London and

Background:The subcutaneous implantable cardioverter-defibrillator(ICD)was designed to avoid complications related to the transvenous ICD lead by using an entirely extrathoracic *** comparing these systems has been based primarily on observational ***:We conducted a noninferiority trial in which patients with an indication for an ICD but no indication for pacing were assigned to receive a subcutaneous ICD or transvenous *** primary end point was the composite of device-related complications and inappropriate shocks;the noninferiority margin for the upper boundary of the 95%confidence interval for the hazard ratio(subcutaneous ICD *** ICD)was 1.45.A superiority analysis was prespecified if noninferiority was established.

关键词： venous Therapy entirely

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