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Editorial
. 2017 Aug 7;21(1):209.
doi: 10.1186/s13054-017-1786-y.

Recovery from critical illness-induced organ failure: the role of autophagy

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Editorial

Recovery from critical illness-induced organ failure: the role of autophagy

Jan Gunst. Crit Care. .

Abstract

Autophagy is a catabolic process by which cells can dispose of damaged content and intracellular microorganisms. Recent evidence implicates autophagy as a crucial repair process necessary to recover from critical illness-induced organ failure. Withholding parenteral nutrition in the acute phase of critical illness activates autophagy and enhances recovery. Several registered drugs have autophagy-stimulating properties, but all lack specificity and none has been investigated in critically ill patients for this purpose.

Keywords: Autophagy; Critical illness; Insulin; Multiple organ dysfunction syndrome; Nutrition; Sepsis.

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Competing interests

The author declares that he has no competing interests.

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Figures

Fig. 1
Fig. 1
Overview of autophagy. Autophagy initiates with the formation of an isolation membrane (also called phagophore) in the cytoplasm. Isolation membranes elongate to finally form a double-membrane vesicle, the autophagosome. During the elongation process, intracellular cargo (e.g., damaged organelles, protein aggregates, invaded microorganisms) is recruited to the isolation membrane to be engulfed. After maturation of the autophagosome, the vesicle fuses with a lysosome, resulting in formation of an autolysosome, in which the sequestered content is degraded and thereafter recycled to the cytoplasm. The figure is original for this article

References

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