Acute lung injury is a life-threatening disease that is characterized by pulmonary inflammation, loss of barrier functions, and hypoxemia. Sphingolipids are critically involved in the disease process that they can both expedite and extenuate: They expedite inflammation by promoting chemotaxis (neutral sphingomyelinase), increased endothelial permeability (acid sphingomyelinase, S1P3-receptors), increased epithelial permeability (S1P2- and S1P3-receptors), and delaying neutrophil apoptosis (neutral sphingomyelinase, S1P1-receptors). They extenuate inflammation by attenuating chemotaxis (S1P) and by stabilizing the endothelial and the epithelial barrier (S1P1-receptor). This chapter discusses the multiple roles and therapeutic options that sphingolipids offer with respect to acute lung injury. © Springer-Verlag Wien 2013.
CITATION STYLE
Uhlig, S., & Yang, Y. (2013). Sphingolipids in acute lung injury. Handbook of Experimental Pharmacology, 216, 227–246. https://doi.org/10.1007/978-3-7091-1511-4_11
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