The change in plasma RIPK3 from presentation to 48 h (ΔRIPK3) was associated with ARDS in sepsis (OR 1.30, 95% CI 1.03-1.63, per ½ standard deviation) and trauma (OR 1.79, 95% CI 1.33-2.40).
In conclusion, using this novel Medical-<i>In silico</i> approach, our data suggest (i) that HS induces necroptosis in cardiomyocytes by phosphorylation (activation) of receptor-interacting protein 3, (ii) that HS is a therapeutic target in trauma- or sepsis-associated cardiomyopathy, and (iii) indicate that this proof-of-concept is a first step toward simulating the extent of activated components in the pro-apoptotic pathway induced by HS with only a small data set gained from the <i>in vitro</i> experiments by using machine learning algorithms.
These results suggested that dynamic monitoring of RIPK3 levels can contribute to the prediction of outcome of sepsis and might be of particular value in identifying patients who would benefit from specific treatments.
Here, we demonstrate that IL-1β production during sepsis with uropathogenic <i>E. coli</i> is mediated by caspase-8, since caspase-8 and RIPK3 double knock out mice show substantially lower cytokine during sepsis and increased survival after injection of TNFα.