Alterations of the Ceramide Metabolism in the Peri-Infarct Cortex Are Independent of the Sphingomyelinase Pathway and Not Influenced by the Acid Sphingomyelinase Inhibitor Fluoxetine

@inproceedings{Brunkhorst2015AlterationsOT,
  title={Alterations of the Ceramide Metabolism in the Peri-Infarct Cortex Are Independent of the Sphingomyelinase Pathway and Not Influenced by the Acid Sphingomyelinase Inhibitor Fluoxetine},
  author={Robert Brunkhorst and Felix Friedl{\"a}nder and Nerea Ferreir{\'o}s and Stephanie Schwalm and Alexander Koch and Georgios Grammatikos and Stefan W Toennes and Christian Foerch and Josef M. Pfeilschifter and Waltraud Pfeilschifter},
  booktitle={Neural plasticity},
  year={2015}
}
Ceramides induce important intracellular signaling pathways, modulating proliferation, migration, apoptosis, and inflammation. However, the relevance of the ceramide metabolism in the reconvalescence phase after stroke is unclear. Besides its well-known property as a selective serotonin reuptake inhibitor, fluoxetine has been reported to inhibit the acid sphingomyelinase (ASM), a key regulator of ceramide levels which derives ceramide from sphingomyelin. Furthermore, fluoxetine has shown… CONTINUE READING

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