Mitochondrial dysfunction and biogenesis: do ICU patients die from mitochondrial failureReport as inadecuate




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Annals of Intensive Care

, 1:41

First Online: 26 September 2011Received: 06 May 2011Accepted: 26 September 2011

Abstract

Mitochondrial functions include production of energy, activation of programmed cell death, and a number of cell specific tasks, e.g., cell signaling, control of Ca metabolism, and synthesis of a number of important biomolecules. As proper mitochondrial function is critical for normal performance and survival of cells, mitochondrial dysfunction often leads to pathological conditions resulting in various human diseases. Recently mitochondrial dysfunction has been linked to multiple organ failure MOF often leading to the death of critical care patients. However, there are two main reasons why this insight did not generate an adequate resonance in clinical settings. First, most data regarding mitochondrial dysfunction in organs susceptible to failure in critical care diseases liver, kidney, heart, lung, intestine, brain were collected using animal models. Second, there is no clear therapeutic strategy how acquired mitochondrial dysfunction can be improved. Only the benefit of such therapies will confirm the critical role of mitochondrial dysfunction in clinical settings. Here we summarized data on mitochondrial dysfunction obtained in diverse experimental systems, which are related to conditions seen in intensive care unit ICU patients. Particular attention is given to mechanisms that cause cell death and organ dysfunction and to prospective therapeutic strategies, directed to recover mitochondrial function. Collectively the data discussed in this review suggest that appropriate diagnosis and specific treatment of mitochondrial dysfunction in ICU patients may significantly improve the clinical outcome.

List of abbreviationsAIFapoptosis-inducing factor

ALIacute lung injury

AMPKAMP-activated protein kinase

ARDSacute respiratory distress syndrome

ATCacute traumatic coagulopathy

DAMPsdamage-associated molecular patterns

ERKextracellular signal-regulated kinases

HKIIIhexokinase III

5-HT5-hydroxytryptamine receptors

I-Rischemia-reperfusion

ICUthe intensive care units

JAKJanus-Kinase

MOFmultiple organ failure

mtDNAmitochondrial DNA

mtTFAmitochondrial transcription factor A

Nrf2factor-E2-related factor

NRFsnuclear respiratory factors

OXPHOSoxidative phosphorylation

P66SHCSrc, homology 2 domain containing transforming protein

PARPpolyADP-ribosepolymerase

PGC-1αproliferator-activated receptor-γ coactivator-1α

Pin 1prolyl-isomerase1

PKAprotein kinase A

PKCprotein kinase C

Rasrat sarcoma

ROSreactive oxygen species

STATsignal transducers and activators of transcription

TLR-4toll-like receptor 4

UCPuncoupling protein.

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Author: Andrey V Kozlov - Soheyl Bahrami - Enrico Calzia - Peter Dungel - Lars Gille - Andrey V Kuznetsov - Jakob Troppmair

Source: https://link.springer.com/



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