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Rocio Salas-Whalen is a board-certified endocrinologist at New York Endocrinology in New York, New York

In agreement with observations made in in vitro models, various findings support the hypothesis that the cardioprotective effects of GLP-1 (736) in ischemia-reperfusion models are mediated by the activation of kinases in the RISK pathway, including PI3K, ERK1/2, cAMP, PKA, Akt, and P70S6K (Table 2).29,34,42,49,50,5255 On the other hand, it has been suggested that the improvement seen after the administration of GLP-1 (736) in MI in terms of increased survival and improved cardiac function could also be due to the decreased activation of inflammatory cells,56 improved myocardial microcirculation,57 and increased myocardial glucose uptake (Fig

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Mechanistically, lipopolysaccharide (LPS)-induced lung injury was less severe and had less neutrophil infiltration and endothelial exudation in sphingosine kinase (SPK)1-/- mice compared to wild type (WT) mice, with decreased numbers of inflammatory cells in theBAL