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Aktivierung der endothelialen Proliferation und Regeneration durch Pentaerithrityltetranitrat (PETN): Funktionelle Konsequenz der Induktion von Hämoxygenase-1

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Pentaerithrityltetranitrat

Zusammenfassung

Bis vor kurzem galt Ferritin als ein Protein, dessen Hauptfunktion in der Speicherung von Eisen liegt und dem ansonsten keine Bedeutung als potentieller Wirkort von Arzneistoffen zukommt. Verschiedene Studien, auch aus unserer Gruppe [1, 9, 17–19], haben aber gezeigt, dass Ferritin bzw. neu synthetisiertes eisenfreies Apoferritin eine Schlüsselfunktion als endogener „iron scavenger“ mit cytoprotektiven Eigenschaften besitzt. Ferritin fungiert dabei als antioxidatives Protein, das dem Prozess der Sauerstoffradikalbildung die als Katalysator essentiellen, freien cytosolischen Eisenionen (Fenton-Chemie) rasch und dauerhaft entzieht. Ferritin erhöht dadurch die Resistenz des Gewebes gegenüber zellschädigenden Einflüssen wie aktivierten Neutrophilen, Wasserstoffsuperoxid oder oxidiertem Low-density-Lipoprotein [1, 6, 17, 18]. Auch klinische Studien weisen darauf hin, dass hohe zelluläre Eisenspiegel oxidativen Stress verursachen und ein koronares Risiko darstellen [26, 30, 31]. Eine Steigerung katalytisch aktiven Eisens gefolgt von vermehrter Ferritinexpression wurde außerdem von verschiedenen Autoren in atherosklerotischen Gefäßläsionen bei Patienten mit koronarer Herzkrankheit beschrieben, ein Befund, der die In-vivo-Relevanz dieses antioxidativen Stoffwechselwegs unterstreicht [8, 22, 28].

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Oberle-Plümpe, S. et al. (2004). Aktivierung der endothelialen Proliferation und Regeneration durch Pentaerithrityltetranitrat (PETN): Funktionelle Konsequenz der Induktion von Hämoxygenase-1. In: Mutschler, E., Zeiher, A.M., Stalleicken, D. (eds) Pentaerithrityltetranitrat. Steinkopff, Heidelberg. https://doi.org/10.1007/978-3-642-87805-3_4

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  • DOI: https://doi.org/10.1007/978-3-642-87805-3_4

  • Publisher Name: Steinkopff, Heidelberg

  • Print ISBN: 978-3-7985-1439-3

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