Abstract
Balloon angioplasty (e. g. PTCA) leads to the activation of a number of genes in injured vessels1. As a consequence of the endothelium damage several characteristic reactions, such as thrombus formation, vasoconstriction and finally - vascular smooth muscle cell (VSMC) proliferation, lead to restenosis1. Among other things, the diminished generation of nitric oxide (NO), due to the lack of constitutively expressed endothelial NO synthase (eNOS) is causatively connected with this process.
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Dembinska-Kiec, A. et al. (1997). Induction of Nitric Oxide Synthase (NOS) and Vascular Endothelial Growth Factor (VEGF) in Experimental Model of Angioplasty and Heart Ischemia. In: Sinzinger, H., Samuelsson, B., Vane, J.R., Paoletti, R., Ramwell, P., Wong, P.YK. (eds) Recent Advances in Prostaglandin, Thromboxane, and Leukotriene Research. Advances in Experimental Medicine and Biology, vol 433. Springer, Boston, MA. https://doi.org/10.1007/978-1-4899-1810-9_33
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DOI: https://doi.org/10.1007/978-1-4899-1810-9_33
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