Editorial Retraction

Puneet, Padmam; Yap, Celestial T.; Wong, Lung Hsiang; Yulin, L.; Koh, Dow Rhoon; Moochhala, Shabbir; Pfeilschifter, Josef; Huwiler, Andrea

doi:10.1126/science.341.6144.342-a

Cited by 1 publication

(1 citation statement)

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“…Whereas some studies have reported that colonic inflammation 26 and synovial inflammation in TNF-induced arthritis 72 are reduced in Sphk1 knockout mice, others have reported that these mice have normal acute and chronic inflammatory responses 73 . The retraction of a paper that suggested SphK1 had a role in regulating pro-inflammatory responses in a mouse sepsis model was concerning 74 , and there is no evidence that inhibiting SphK1 or deleting its gene will reduce sepsis. Although Sphk2 knockout mice have normal neutrophil functions, in a model of bacterial lung infection these mice have accelerated disease progression 75 .…”

Section: Sphingolipids and Inflammationmentioning

confidence: 99%

Sphingolipid metabolites in inflammatory disease

Maceyka

Spiegel

2014

Nature

980

925

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Sphingolipids are ubiquitous building blocks of eukaryotic cell membranes. Progress in our understanding of sphingolipid metabolism, state-of-the-art sphingolipidomic approaches and animal models have generated a large body of evidence demonstrating that sphingolipid metabolites, particularly ceramide and sphingosine-1-phosphate, are signalling molecules that regulate a diverse range of cellular processes that are important in immunity, inflammation and inflammatory disorders. Recent insights into the molecular mechanisms of action of sphingolipid metabolites and new perspectives on their roles in regulating chronic inflammation have been reported. The knowledge gained in this emerging field will aid in the development of new therapeutic options for inflammatory disorders.

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