HMG-CoA reductase inhibitors (statins) increase endothelial progenitor cells via the PI 3-kinase/Akt pathway.
By Stefanie Dimmeler, Alexandra Aicher, M. Vasa, Christiane Mildner-Rihm, K. Adler, M. Tiemann, H. Rütten, S. Fichtlscherer, H. Martin, A. Zeiher. Journal of Clinical Investigation, 2001
1,257 citations recorded by the source corpus.
Subfields: Genetics, Hematology, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/04c117082dc2a14d252c35810610e6a8aadd2548
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Citations in the corpus
- Pleiotropic effects of statins. (2005, background): “STATINS AND ENDOTHELIAL PROGENITOR CELLS Statins have also been found to increase the number of circulating endothelial progenitor cells (EPCs) (69).”
- Adult hematopoietic stem cells provide functional hemangioblast activity during retinal neovascularization (2002, background): “Recently, it was demonstrated that hydroxymethylglutaryl (HMG)-CoA reductase inhibitors potently augment EPC differentiation by a mechanism involving the angiogenic protein kinase Akt (ref”
- Therapeutic stem and progenitor cell transplantation for organ vascularization and regeneration (2003, background): “Remarkably, 3-hydroxyl-3-methyl coenzyme A reductase inhibitors (statins) promote incorporation of EPCs into neoangiogenic site”
- Soluble factors released by endothelial progenitor cells promote migration of endothelial cells and cardiac resident progenitor cells. (2005, background): “These endothelial progenitor cells are positive for endothelial marker proteins such as VEGF receptor 2 (KDR), von Willebrand factor (vWF), VE-cadherin, eNOS, take-up of diacetylated LDL, and bind lectin [5–7].”