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2018 ; 2018
(ä): 3646725
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Ceramide and Ischemia/Reperfusion Injury
#MMPMID29610685
He X
; Schuchman EH
J Lipids
2018[]; 2018
(ä): 3646725
PMID29610685
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Ceramide, a bioactive membrane sphingolipid, functions as an important second
messenger in apoptosis and cell signaling. In response to stresses, it may be
generated by de novo synthesis, sphingomyelin hydrolysis, and/or recycling of
complex sphingolipids. It is cleared from cells through the activity of
ceramidases, phosphorylation to ceramide-1-phosphate, or resynthesis into more
complex sphingolipids. Ischemia/reperfusion (IR) injury occurs when
oxygen/nutrition is rapidly reintroduced into ischemic tissue, resulting in cell
death and tissue damage, and is a major concern in diverse clinical settings,
including organ resection and transplantation. Numerous reports show that
ceramide levels are markedly elevated during IR. Mitochondria are major sites of
reactive oxygen species (ROS) production and play a key role in IR-induced and
ceramide-mediated cell death and tissue damage. During the development of IR
injury, the initial response of ROS and TNF-alpha production activates two major
ceramide generating pathways (sphingomyelin hydrolysis and de novo ceramide
synthesis). The increased ceramide has broad effects depending on the IR phases,
including both pro- and antiapoptotic effects. Therefore, strategies that reduce
the levels of ceramide, for example, by modulation of ceramidase and/or
sphingomyelinases activities, may represent novel and promising therapeutic
approaches to prevent or treat IR injury in diverse clinical settings.
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