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Wirkmechanismus laut Studien BPC-157 — VEGFR2-Akt-eNOS-Achse: In humanen Endothelzellen und im Rattenmodell der Hinterlaufischämie stiegen VEGFR2-Expression und -Internalisierung, die Gefäßdichte nahm zu, die Durchblutung erholte sich schneller
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