H
Hans W.M. Niessen
Researcher at VU University Medical Center
Publications - 224
Citations - 13218
Hans W.M. Niessen is an academic researcher from VU University Medical Center. The author has contributed to research in topics: Myocardial infarction & Inflammation. The author has an hindex of 49, co-authored 203 publications receiving 11303 citations. Previous affiliations of Hans W.M. Niessen include VU University Amsterdam & Indian Council of Agricultural Research.
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Journal ArticleDOI
Myocardial infarction accelerates atherosclerosis
Partha Dutta,Gabriel Courties,Ying Wei,Florian Leuschner,Florian Leuschner,Rostic Gorbatov,Clinton S. Robbins,Yoshiko Iwamoto,Brian Thompson,Alicia L. Carlson,Timo Heidt,Maulik D. Majmudar,Maulik D. Majmudar,Felix Lasitschka,Martin Etzrodt,Peter Waterman,Michael T. Waring,Michael T. Waring,Adam T. Chicoine,Adam T. Chicoine,Anja M. van der Laan,Hans W.M. Niessen,Jan J. Piek,Barry B. Rubin,Jagdish Butany,James R. Stone,Hugo A. Katus,Sabina A. Murphy,David A. Morrow,Marc S. Sabatine,Claudio Vinegoni,Michael A. Moskowitz,Mikael J. Pittet,Peter Libby,Charles P. Lin,Filip K. Swirski,Ralph Weissleder,Matthias Nahrendorf +37 more
TL;DR: It is shown that the systemic response to ischaemic injury aggravates chronic atherosclerosis and provides a novel therapeutic opportunity to mitigate disease progression.
Journal ArticleDOI
C-Reactive Protein as a Cardiovascular Risk Factor More Than an Epiphenomenon?
Wim K. Lagrand,Cees A. Visser,Wim Th. Hermens,Hans W.M. Niessen,Freek W.A. Verheugt,Gertjan Wolbink,C. E. Hack +6 more
TL;DR: It is hypothesized that CRP may directly interact with atherosclerotic vessels or ischemic myocardium by activation of the complement system, thereby promoting inflammation and thrombosis and may provide new directions for prevention of cardiovascular events.
Journal ArticleDOI
Myocardial structure and function differ in systolic and diastolic heart failure.
Loek van Heerebeek,Attila Borbély,Hans W.M. Niessen,Jean G.F. Bronzwaer,Jolanda van der Velden,Ger J.M. Stienen,Wolfgang A. Linke,Gerrit J Laarman,Walter Paulus +8 more
TL;DR: LV myocardial structure and function differ in SHF and DHF because of distinct cardiomyocyte abnormalities, and these findings support the clinical separation of heart failure patients into SHF or DHF phenotypes.
Journal ArticleDOI
Diastolic Stiffness of the Failing Diabetic Heart Importance of Fibrosis, Advanced Glycation End Products, and Myocyte Resting Tension
Loek van Heerebeek,Nazha Hamdani,M. Louis Handoko,Inês Falcão-Pires,René J. P. Musters,Koba Kupreishvili,Alexander Ijsselmuiden,Casper G. Schalkwijk,Jean G.F. Bronzwaer,Michaela Diamant,Attila Borbély,Jolanda van der Velden,Ger J.M. Stienen,Gerrit J Laarman,Hans W.M. Niessen,Walter Paulus +15 more
TL;DR: Mechanisms responsible for the increased diastolic stiffness of the diabetic heart differ in heart failure with reduced and normal LVEF: Fibrosis and AGEs are more important when LveF is reduced, whereas cardiomyocyte resting tension is more importantWhen LVEf is normal.
Journal ArticleDOI
Human bone marrow- and adipose-mesenchymal stem cells secrete exosomes enriched in distinctive miRNA and tRNA species.
Serena Rubina Baglìo,Koos Rooijers,Danijela Koppers-Lalic,Frederik J. Verweij,M Pérez Lanzón,Nicoletta Zini,B.A. Naaijkens,Francesca Perut,Hans W.M. Niessen,Nicola Baldini,D. Michiel Pegtel +10 more
TL;DR: It is demonstrated that primary MSCs release small RNAs via exosomes, which are increasingly implicated in intercellular communications, and may help to understand how M SCs impact neighboring or distant cells with possible consequences for their therapeutic usage.