The Signaling Network Resulting in Ventilator-induced Diaphragm Dysfunction

American Journal of Respiratory Cell and Molecular Biology
Huibin Tang, Joseph B Shrager

Abstract

Mechanical ventilation (MV) is a life-saving measure for those incapable of adequately ventilating or oxygenating without assistance. Unfortunately, even brief periods of MV result in diaphragm weakness (i.e., ventilator-induced diaphragm dysfunction [VIDD]) that may render it difficult to wean the ventilator. Prolonged MV is associated with cascading complications and is a strong risk factor for death. Thus, prevention of VIDD may have a dramatic impact on mortality rates. Here, we summarize the current understanding of the pathogenic events underlying VIDD. Numerous alterations have been proven important in both human and animal MV diaphragm. These include protein degradation via the ubiquitin proteasome system, autophagy, apoptosis, and calpain activity-all causing diaphragm muscle fiber atrophy, altered energy supply via compromised oxidative phosphorylation and upregulation of glycolysis, and also mitochondrial dysfunction and oxidative stress. Mitochondrial oxidative stress in fact appears to be a central factor in each of these events. Recent studies by our group and others indicate that mitochondrial function is modulated by several signaling molecules, including Smad3, signal transducer and activator of transcription 3...Continue Reading

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Citations

Jul 28, 2019·Intensive Care Medicine Experimental·Oscar PeñuelasJosé Ángel Lorente
Nov 21, 2018·Experimental Biology and Medicine·Yung-Yang Liu, Li-Fu Li
Aug 25, 2021·Therapeutic Advances in Respiratory Disease·Hui YongJicheng Wei

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Methods Mentioned

BETA
ubiquitination
biopsies
nuclear translocation

Software Mentioned

DAVID

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