Published in:
Open Access
01-02-2011 | Poster presentation
Insufficient activation of autophagy allows accumulation of cellular damage and may contribute to sustained organ failure in prolonged critically ill patients
Authors:
J Gunst, S Derde, I Derese, M Boussemaere, F Güiza, W Martinet, JP Timmermans, A D'Hoore, PJ Wouters, G Van den Berghe, I Vanhorebeek
Published in:
Critical Care
|
Special Issue 1/2011
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Excerpt
Prolonged critically ill patients face a high risk of death, which is most often due to nonresolving multiple organ failure and muscle weakness. Increased oxidative stress, accumulation of damaged proteins and mitochondrial dysfunction contribute to cellular and organ dysfunction, and persistence of these abnormalities may trigger additional damage. Autophagy is the only degradation pathway able to remove toxic protein aggregates and damaged mitochondria. Feeding and insulin are two powerful suppressors of autophagy. We therefore hypothesized that in fed, prolonged critically ill patients receiving insulin, the required activation of autophagy to clear cellular damage could be impaired. …
