Thorsten Kessler

ORCID: 0000-0003-3326-1621
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About
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Research Areas
  • Genetic Associations and Epidemiology
  • Atherosclerosis and Cardiovascular Diseases
  • Cardiac Valve Diseases and Treatments
  • Coronary Interventions and Diagnostics
  • Lipoproteins and Cardiovascular Health
  • Antiplatelet Therapy and Cardiovascular Diseases
  • Cardiovascular Function and Risk Factors
  • RNA modifications and cancer
  • Cardiac Fibrosis and Remodeling
  • Acute Myocardial Infarction Research
  • Cardiac Imaging and Diagnostics
  • Cell Adhesion Molecules Research
  • Protease and Inhibitor Mechanisms
  • Cancer-related molecular mechanisms research
  • Lipid metabolism and disorders
  • Phosphodiesterase function and regulation
  • Infective Endocarditis Diagnosis and Management
  • Nuclear Receptors and Signaling
  • Renin-Angiotensin System Studies
  • Cardiomyopathy and Myosin Studies
  • Receptor Mechanisms and Signaling
  • Bioinformatics and Genomic Networks
  • Cardiovascular Disease and Adiposity
  • Nitric Oxide and Endothelin Effects
  • Signaling Pathways in Disease

Deutsches Herzzentrum München
2016-2025

German Centre for Cardiovascular Research
2016-2025

Technical University of Munich
2016-2025

University of California, Los Angeles
2017-2022

University of Münster
1994-2022

München Klinik
2014-2021

ORCID
2021

Deutsches Herzzentrum der Charité
2014-2017

University of Lübeck
2011-2017

University of Tartu
2017

Panos Deloukas Stavroula Kanoni Christina Willenborg Martin Farrall Themistocles L. Assimes and 95 more John R. Thompson Erik Ingelsson Danish Saleheen Jeanette Erdmann Benjamin A. Goldstein Kathleen Stirrups Inke R. König Jean‐Baptiste Cazier Åsa Johansson Alistair S. Hall Jong‐Young Lee Cristen J. Willer John C. Chambers Tõnu Esko Lasse Folkersen Anuj Goel Elin Grundberg Aki S. Havulinna Weang-Kee Ho Jemma C. Hopewell Niclas Eriksson Marcus E. Kleber Kati Kristiansson Per Lundmark Leo‐Pekka Lyytikäinen Suzanne Rafelt Dmitry Shungin Rona J. Strawbridge Guðmar Þorleifsson Emmi Tikkanen Natalie Van Zuydam Benjamin F. Voight Lindsay L. Waite Weihua Zhang Andreas Ziegler Devin Absher David Altshuler Anthony J. Balmforth Inês Barroso Peter S. Braund Christof Burgdorf Xueling Sim David Cox Maria Dimitriou Ron Do Alex S. F. Doney NourEddine El Mokhtari Per Eriksson Krista Fischer Pierre Fontanillas Anders Franco‐Cereceda Bruna Gigante Per‐Henrik Groop Stefan Gustafsson Jörg Hager Göran Hallmans Bok-Ghee Han Sarah Hunt Hyun Min Kang Thomas Illig Thorsten Kessler Joshua Knowles Genovefa Kolovou Johanna Kuusisto Claudia Langenberg Cordelia Langford Karin Leander Marja‐Liisa Lokki Anders Lundmark Mark I. McCarthy Christa Meisinger Olle Melander Evelin Mihailov Seraya Maouche Andrew D. Morris Martina Müller‐Nurasyid Kjell Nikus John F. Peden Nigel W. Rayner Asif Rasheed Silke Rosinger Deborah C. Rubin Moritz Rumpf Arne Schäfer Mohan U. Sivananthan Ci Song Alexandre F.R. Stewart Sian-Tsung Tan Guðmundur Þorgeirsson C. Ellen van der Schoot Peter J. Wagner George A. Wells Philipp S. Wild Tsun-Po Yang Philippe Amouyel

10.1038/ng.2480 article EN Nature Genetics 2012-12-02

Ezetimibe lowers plasma levels of low-density lipoprotein (LDL) cholesterol by inhibiting the activity Niemann-Pick C1-like 1 (NPC1L1) protein. However, whether such inhibition reduces risk coronary heart disease is not known. Human mutations that inactivate a gene encoding drug target can mimic action an inhibitory and thus be used to infer potential effects drug.We sequenced exons NPC1L1 in 7364 patients with 14,728 controls without who were European, African, or South Asian ancestry. We...

10.1056/nejmoa1405386 article EN New England Journal of Medicine 2014-11-12
Tom R. Webb Jeanette Erdmann Kathleen Stirrups Nathan O. Stitziel Nicholas G. D. Masca and 95 more Henning Jansen Stavroula Kanoni Christopher P. Nelson Paola G. Ferrario Inke R. König John D. Eicher Andrew D. Johnson Stephen E. Hamby Christer Betsholtz Arno Ruusalepp Oscar Franzén Eric E. Schadt Johan Björkegren Peter Weeke Paul L. Auer Ursula M. Schick Yingchang Lu He Zhang Marie‐Pierre Dubé Anuj Goel Martin Farrall Gina M. Peloso Hong‐Hee Won Ron Do Erik Van Iperen Jochen Kruppa Anubha Mahajan Robert A. Scott Christina Willenborg Peter S. Braund Julian C. van Capelleveen Alex S. F. Doney Louise A. Donnelly Rosanna Asselta Pier Angelica Merlini Stefano Duga Nicola Marziliano Joshua C. Denny Christian M. Shaffer Nour Eddine El-Mokhtari André Franke Stefanie Heilmann‐Heimbach Christian Hengstenberg Per Hoffmann Oddgeir L. Holmen Kristian Hveem Jan-Håkan Jansson Karl‐Heinz Jöckel Thorsten Kessler Jennifer Kriebel Karl‐Ludwig Laugwitz Eirini Marouli Nicola Martinelli Mark I. McCarthy Natalie R. van Zuydam Christa Meisinger Tõnu Esko Evelin Mihailov Stefan Andersson Escher Maris Alver Susanne Moebus Andrew D. Morris Jarma Virtamo Majid Nikpay Oliviero Olivieri Sylvie Provost Alaa AlQarawi Neil R. Robertson Karen O. Akinsansya Dermot F. Reilly Thomas Vogt Wu Yin Folkert W. Asselbergs Charles Kooperberg Rebecca D. Jackson Eli A. Stahl Martina Müller‐Nurasyid Konstantin Strauch Tibor V. Varga Mélanie Waldenberger Lingyao Zeng Rajiv Chowdhury Veikko Salomaa Ian Ford J. Wouter Jukema Philippe Amouyel Jukka Kontto Børge G. Nordestgaard Jean Ferrières Danish Saleheen Naveed Sattar Praveen Surendran Aline Wagner Robin Young Joanna M. M. Howson

Genome-wide association studies have so far identified 56 loci associated with risk of coronary artery disease (CAD). Many CAD show pleiotropy; that is, they are also other diseases or traits. This study sought to systematically test if genetic variants for non-CAD diseases/traits associate and undertake a comprehensive analysis the extent pleiotropy all loci. In discovery analyses involving 42,335 cases 78,240 control subjects we tested 29,383 common (minor allele frequency >5%) single...

10.1016/j.jacc.2016.11.056 article EN cc-by Journal of the American College of Cardiology 2017-02-01

<h3>Importance</h3> The activity of lipoprotein lipase (LPL) is the rate-determining step in clearing triglyceride-rich lipoproteins from circulation. Mutations that damage LPL gene (<i>LPL</i>) lead to lifelong deficiency enzymatic and can provide insight into relationship human disease. <h3>Objective</h3> To determine whether rare and/or common variants in<i>LPL</i>are associated with early-onset coronary artery disease (CAD). <h3>Design, Setting, Participants</h3> In a cross-sectional...

10.1001/jama.2017.0972 article EN JAMA 2017-03-07

Heart failure following myocardial infarction (MI) remains one of the major causes death worldwide, and its treatment is a crucial challenge cardiovascular medicine. An attractive therapeutic strategy to stimulate endogenous mechanisms regeneration. This study evaluates potential with annexin A1 (AnxA1) induce cardiac repair after MI. AnxA1 knockout (AnxA1−/−) wild-type mice underwent MI induced by ligation left anterior descending coronary artery. Cardiac functionality was assessed...

10.1016/j.jacc.2019.03.503 article EN cc-by-nc-nd Journal of the American College of Cardiology 2019-06-01

Abstract Aims The best interventional strategy for the treatment of drug-eluting stent (DES) in-stent restenosis (ISR) is still unclear and no data from randomized trials beyond 3-year follow-up are available. We aimed to define 10-year comparative efficacy safety plain balloon (PB), paclitaxel-coated (PCB), paclitaxel-eluting (PES) percutaneous coronary intervention (PCI) DES-ISR. Methods results Clinical patients randomly assigned PB, PCB, PES in ISAR-DESIRE 3 trial was extended 10 years...

10.1093/eurheartj/ehad026 article EN European Heart Journal 2023-02-21

Background— ADAMTS-7, a member of the disintegrin and metalloproteinase with thrombospondin motifs (ADAMTS) family, was recently identified to be significantly associated genomewide coronary artery disease. However, mechanisms that link ADAMTS-7 disease risk remain elusive. We have previously demonstrated promotes vascular smooth muscle cell migration postinjury neointima formation via degradation matrix protein cartilage oligomeric protein. Because delayed endothelium repair renders...

10.1161/circulationaha.114.014072 article EN Circulation 2015-02-26
Daniel F. Freitag Adam S. Butterworth Peter Willeit Joanna M. M. Howson Stephen Burgess and 95 more Stephen Kaptoge Robin Young Weang-Kee Ho Angela Wood Michael Sweeting Sarah Spackman James R Staley Anna Ramond Eric L. Harshfield Sune F. Nielsen Peer Grande Leslie A. Lange Matthew J. Bown Gregory T. Jones Robert A. Scott Steve Bevan Eleonora Porcu Gudmar Thorleifsson Lingyao Zeng Thorsten Kessler Majid Nikpay Ron Do Weihua Zhang Jemma C. Hopewell Marcus E. Kleber Graciela E. Delgado Christopher P. Nelson Anuj Goel Joshua C. Bis Abbas Dehghan Symen Ligthart Albert V. Smith Liming Qu Femke N. G. van ’t Hof P. Bakker Annette F. Baas André van Rij Gerard Tromp Helena Kuivaniemi Marylyn D. Ritchie Shefali S. Verma Dana C. Crawford Jennifer Malinowski Mariza de Andrade Iftikhar J. Kullo Peggy Peissig Catherine A. McCarty Erwin P. Böttinger Omri Gottesman David R. Crosslin David Carrell Laura J. Rasmussen‐Torvik Jennifer A. Pacheco Jie Huang Nicholas J. Timpson Johannes Kettunen Mika Ala‐Korpela Gary F. Mitchell Afshin Parsa Ian B. Wilkinson Mathias Gorski Yong Li Nora Franceschini Margaux F. Keller Santhi K. Ganesh Carl D. Langefeld Lucie Bruijn Matthew A. Brown David M. Evans Svetlana Baltic Manuel A. R. Ferreira Hansjörg Baurecht Stephan Weidinger Andre Franke Steven A. Lubitz Martina Müller‐Nurasyid Janine F. Felix Nicholas Smith Marc Sudman Susan D. Thompson Eleftheria Zeggini Kalliope Panoutsopoulou Mike A. Nalls Andrew Singleton Constantin Polychronakos Jonathan P. Bradfield Hákon Hákonarson Douglas F. Easton Deborah J. Thompson Ian Tomlinson Malcolm G. Dunlop Kari Hemminki Gareth J. Morgan Timothy Eisen Hartmut Goldschmidt

To investigate potential cardiovascular and other effects of long-term pharmacological interleukin 1 (IL-1) inhibition, we studied genetic variants that produce inhibition IL-1, a master regulator inflammation. We created score combining the alleles two common (rs6743376 rs1542176) are located upstream IL1RN, gene encoding IL-1 receptor antagonist (IL-1Ra; an endogenous inhibitor both IL-1α IL-1β); increase soluble IL-1Ra protein concentration. compared on inflammation biomarkers this with...

10.1016/s2213-8587(15)00034-0 article EN cc-by-nc-nd The Lancet Diabetes & Endocrinology 2015-02-26

Background: A chromosomal locus at 4q32.1 has been genome-wide significantly associated with coronary artery disease risk. The encompasses GUCY1A3 , which encodes the α 1 subunit of soluble guanylyl cyclase (sGC), a key enzyme in nitric oxide/cGMP signaling pathway. mechanism linking common variants this region risk is not known. Methods: Gene expression and protein were analyzed quantitative polymerase chain reaction immunoblotting, respectively. Putative allele-specific transcription...

10.1161/circulationaha.116.024152 article EN Circulation 2017-05-10

Abstract Aims Mental stress substantially contributes to the initiation and progression of human disease, including cardiovascular conditions. We aim investigate underlying mechanisms these contributions since they remain largely unclear. Methods results Here, we show in humans mice that leucocytes deplete rapidly from blood after a single episode acute mental stress. Using cell-tracking experiments animal models stress, found exposure leads prompt uptake inflammatory distinct tissues heart,...

10.1093/eurheartj/ehab371 article EN cc-by-nc European Heart Journal 2021-06-03

Abstract Aims Targeting vascular inflammation represents a novel therapeutic approach to reduce complications of atherosclerosis. Neutralizing the pro-inflammatory cytokine interleukin-1β (IL-1β) using canakinumab, monoclonal antibody, reduces incidence cardiovascular events in patients after myocardial infarction (MI). The biological basis for these beneficial effects remains incompletely understood. We sought explore mechanisms IL-1β-targeted therapies. Methods and results In mice with...

10.1093/cvr/cvab337 article EN cc-by-nc Cardiovascular Research 2021-10-25

The majority of risk loci identified by genome-wide association studies (GWAS) are in non-coding regions, hampering their functional interpretation. Instead, transcriptome-wide (TWAS) identify gene-trait associations, which can be used to prioritize candidate genes disease-relevant tissue(s). Here, we aimed systematically susceptibility for coronary artery disease (CAD) TWAS. We trained prediction models nine CAD-relevant tissues using EpiXcan based on two genetics-of-gene-expression panels,...

10.1007/s00395-022-00917-8 article EN cc-by Basic Research in Cardiology 2022-02-17
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