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Parathyroid hormone treatment after myocardial infarction promotes cardiac repair by enhanced neovascularization and cell survival
Author(s) -
MarcMichael Zaruba,
Bruno Hüber,
Stefan Brunner,
Elisabeth Deindl,
Robert David,
R Fischer,
Gerald Assmann,
Nadja Herbach,
Sebastian Grundmann,
Rüdiger Wanke,
Josef MuellerHoecker,
WolfgangMichael Franz
Publication year - 2007
Publication title -
cardiovascular research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.774
H-Index - 219
eISSN - 1755-3245
pISSN - 0008-6363
DOI - 10.1093/cvr/cvm080
Subject(s) - medicine , parathyroid hormone , neovascularization , stem cell , progenitor cell , myocardial infarction , endocrinology , cd34 , angiogenesis , vascular endothelial growth factor , cardiology , calcium , biology , vegf receptors , genetics
An ongoing concept is that stem cells have the potential to regenerate the injured myocardium. In addition to direct vasorelaxing effects on the vasculature, which are mediated by an increased cAMP production leading to a decreased calcium influx in smooth muscle cells, parathyroid hormone (PTH) was recently shown to facilitate stem cell mobilization. Therefore, we analysed in a murine model of experimental myocardial infarction (MI) the influence of PTH treatment on survival, functional parameters, stem cell migration, and expression of vascular endothelial growth factor A (VEGF-A).

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