PMID- 24905734
OWN - NLM
STAT- MEDLINE
DCOM- 20140925
LR  - 20240507
IS  - 0006-3002 (Print)
IS  - 0006-3002 (Linking)
VI  - 1842
IP  - 9
DP  - 2014 Sep
TI  - Energy crisis: the role of oxidative phosphorylation in acute inflammation and 
      sepsis.
PG  - 1579-86
LID - S0925-4439(14)00159-8 [pii]
LID - 10.1016/j.bbadis.2014.05.031 [doi]
AB  - Mitochondrial dysfunction is increasingly recognized as an accomplice in most of 
      the common human diseases including cancer, neurodegeneration, diabetes, 
      ischemia/reperfusion injury as seen in myocardial infarction and stroke, and 
      sepsis. Inflammatory conditions, both acute and chronic, have recently been shown 
      to affect mitochondrial function. We here discuss the role of oxidative 
      phosphorylation (OxPhos), focusing on acute inflammatory conditions, in 
      particular sepsis and experimental sepsis models. We discuss mitochondrial 
      alterations, specifically the suppression of oxidative metabolism and the role of 
      mitochondrial reactive oxygen species in disease pathology. Several signaling 
      pathways including metabolic, proliferative, and cytokine signaling affect 
      mitochondrial function and appear to be important in inflammatory disease 
      conditions. Cytochrome c oxidase (COX) and cytochrome c, the latter of which 
      plays a central role in apoptosis in addition to mitochondrial respiration, serve 
      as examples for the entire OxPhos system since they have been studied in more 
      detail with respect to cell signaling. We propose a model in which inflammatory 
      signaling leads to changes in the phosphorylation state of mitochondrial 
      proteins, including Tyr304 phosphorylation of COX catalytic subunit I. This 
      results in an inhibition of OxPhos, a reduction of the mitochondrial membrane 
      potential, and consequently a lack of energy, which can cause organ failure and 
      death as seen in septic patients.
CI  - Copyright (c) 2014. Published by Elsevier B.V.
FAU - Lee, Icksoo
AU  - Lee I
AD  - College of Medicine, Dankook University, Cheonan-si, Chungcheongnam-do 330-714, 
      Republic of Korea.
FAU - Huttemann, Maik
AU  - Huttemann M
AD  - Center for Molecular Medicine and Genetics, Wayne State University, Detroit, MI 
      48201, USA; Cardiovascular Research Institute, Wayne State University, Detroit, 
      MI 48201, USA; Department of Biochemistry and Molecular Biology, Wayne State 
      University, Detroit, MI 48201, USA; Karmanos Cancer Institute, Detroit, MI 48201, 
      USA. Electronic address: mhuttema@med.wayne.edu.
LA  - eng
GR  - R01 GM089900/GM/NIGMS NIH HHS/United States
GR  - GM089900/GM/NIGMS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PT  - Review
DEP - 20140604
PL  - Netherlands
TA  - Biochim Biophys Acta
JT  - Biochimica et biophysica acta
JID - 0217513
SB  - IM
MH  - Animals
MH  - *Cell Respiration
MH  - *Energy Metabolism
MH  - Humans
MH  - Inflammation/etiology/metabolism/*pathology
MH  - Mitochondria/metabolism/*pathology
MH  - *Oxidative Phosphorylation
MH  - Sepsis/etiology/metabolism/*pathology
PMC - PMC4147665
MID - NIHMS616975
OTO - NOTNLM
OT  - Cytochrome c oxidase
OT  - Electron transport chain
OT  - Haplogroup
OT  - Inflammation
OT  - Mitochondria
OT  - Reactive oxygen species
EDAT- 2014/06/07 06:00
MHDA- 2014/09/26 06:00
PMCR- 2015/09/01
CRDT- 2014/06/07 06:00
PHST- 2014/01/15 00:00 [received]
PHST- 2014/04/17 00:00 [revised]
PHST- 2014/05/27 00:00 [accepted]
PHST- 2014/06/07 06:00 [entrez]
PHST- 2014/06/07 06:00 [pubmed]
PHST- 2014/09/26 06:00 [medline]
PHST- 2015/09/01 00:00 [pmc-release]
AID - S0925-4439(14)00159-8 [pii]
AID - 10.1016/j.bbadis.2014.05.031 [doi]
PST - ppublish
SO  - Biochim Biophys Acta. 2014 Sep;1842(9):1579-86. doi: 
      10.1016/j.bbadis.2014.05.031. Epub 2014 Jun 4.