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Rainer Krebs

Researcher at University of Helsinki

Publications -  67
Citations -  1244

Rainer Krebs is an academic researcher from University of Helsinki. The author has contributed to research in topics: Transplantation & Heart transplantation. The author has an hindex of 17, co-authored 53 publications receiving 1134 citations. Previous affiliations of Rainer Krebs include Helsinki University Central Hospital.

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Vascular endothelial growth factor enhances cardiac allograft arteriosclerosis.

TL;DR: Results in rat cardiac allografts established alloimmune response as an alternative stimulus capable of inducing vascular endothelial growth factor mRNA and protein expression in cardiomyocytes and graft-infiltrating mononuclear inflammatory cells, which suggests that these cells may function as a source of VEGF to the cells of coronary arteries.
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Targeting Lymphatic Vessel Activation and CCL21 Production by Vascular Endothelial Growth Factor Receptor-3 Inhibition Has Novel Immunomodulatory and Antiarteriosclerotic Effects in Cardiac Allografts

TL;DR: Results show that VEGFR-3 participates in immune cell traffic from peripheral tissues to secondary lymphoid organs by regulating allograft lymphatic vessel CCL21 production and suggest VEG FR-3 inhibition as a novel lymphatic vessels–targeted immunomodulatory therapy for cardiac allografted rejection and arteriosclerosis.
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Angiopoietin-1 Protects Against the Development of Cardiac Allograft Arteriosclerosis

TL;DR: The findings suggest that the antiinflammatory properties of Ang1 may offer an entirely new therapeutic approach to prevent cardiac allograft arteriosclerosis.
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Donor Simvastatin Treatment Abolishes Rat Cardiac Allograft Ischemia/Reperfusion Injury and Chronic Rejection Through Microvascular Protection

TL;DR: It is demonstrated that donor simvastatin treatment prevents microvascular endothelial cell and pericyte dysfunction, ischemia/reperfusion injury, and chronic rejection and suggest a novel, clinically feasible strategy to protect cardiac allografts.
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A dose-dependent inhibitory effect of cyclosporine A on obliterative bronchiolitis of rat tracheal allografts.

TL;DR: It is suggested that an acute alloimmune response to airway targets, perhaps to epithelium, is the primary cause of OB, since CsA, with a nearly exclusive effect on the transcription of immune cytokines, entirely inhibited the generation of OB.