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Joost P.G. Sluijter

Researcher at Utrecht University

Publications -  241
Citations -  13201

Joost P.G. Sluijter is an academic researcher from Utrecht University. The author has contributed to research in topics: Progenitor cell & Heart failure. The author has an hindex of 53, co-authored 210 publications receiving 10469 citations. Previous affiliations of Joost P.G. Sluijter include University of Groningen & University Medical Center.

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Correction: Corrigendum: Gap junctional protein Cx43 is involved in the communication between extracellular vesicles and mammalian cells

TL;DR: It is shown that Connexin 43 (Cx43), the most widely expressed GJ protein, is present in exosomes in the form of hexameric channels and, more importantly, that exosomal Cx43 is able to modulate the interaction and transfer of information between exosome and acceptor cells.
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Inhibition of miR-25 improves cardiac contractility in the failing heart

TL;DR: High-throughput functional screening of the human microRNAome reveals that increased expression of endogenous miR-25 contributes to declining cardiac function during heart failure and suggests that it might be targeted therapeutically to restore function.
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Cardiac tissue engineering using tissue printing technology and human cardiac progenitor cells.

TL;DR: This study evaluated the combination of TP, human cardiac-derived cardiomyocyte progenitor cells (hCMPCs) and biomaterials to obtain a construct with cardiogenic potential for in vitro use or in vivo application and showed that printing can be used for defined cell delivery, while retaining functional properties.
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Toll-Like Receptor 4 Mediates Maladaptive Left Ventricular Remodeling and Impairs Cardiac Function After Myocardial Infarction

TL;DR: Data provide direct evidence for a causal role of TLR4 in postinfarct maladaptive LV remodeling, probably via inflammatory cytokine production and matrix degradation and may therefore constitute a novel target in the treatment of ischemic heart failure.
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MicroRNA-1 and -499 Regulate Differentiation and Proliferation in Human-Derived Cardiomyocyte Progenitor Cells

TL;DR: By modulating miR-1 and -499 expression levels, human CMPC function can be altered and differentiation directed, thereby enhancing cardiomyogenic differentiation.