PMID- 23311665
OWN - NLM
STAT- MEDLINE
DCOM- 20140203
LR  - 20240420
IS  - 1557-7716 (Electronic)
IS  - 1523-0864 (Print)
IS  - 1523-0864 (Linking)
VI  - 19
IP  - 6
DP  - 2013 Aug 20
TI  - Redox control of inflammation in macrophages.
PG  - 595-637
LID - 10.1089/ars.2012.4785 [doi]
AB  - Macrophages are present throughout the human body, constitute important immune 
      effector cells, and have variable roles in a great number of pathological, but 
      also physiological, settings. It is apparent that macrophages need to adjust 
      their activation profile toward a steadily changing environment that requires 
      altering their phenotype, a process known as macrophage polarization. Formation 
      of reactive oxygen species (ROS), derived from NADPH-oxidases, mitochondria, or 
      NO-producing enzymes, are not necessarily toxic, but rather compose a network 
      signaling system, known as redox regulation. Formation of redox signals in 
      classically versus alternatively activated macrophages, their action and 
      interaction at the level of key targets, and the resulting physiology still are 
      insufficiently understood. We review the identity, source, and biological 
      activities of ROS produced during macrophage activation, and discuss how they 
      shape the key transcriptional responses evoked by hypoxia-inducible transcription 
      factors, nuclear-erythroid 2-p45-related factor 2 (Nrf2), and peroxisome 
      proliferator-activated receptor-gamma. We summarize the mechanisms how redox signals 
      add to the process of macrophage polarization and reprogramming, how this is 
      controlled by the interaction of macrophages with their environment, and 
      addresses the outcome of the polarization process in health and disease. Future 
      studies need to tackle the option whether we can use the knowledge of redox 
      biology in macrophages to shape their mediator profile in pathophysiology, to 
      accelerate healing in injured tissue, to fight the invading pathogens, or to 
      eliminate settings of altered self in tumors.
FAU - Brune, Bernhard
AU  - Brune B
AD  - Faculty of Medicine, Institute of Biochemistry I-Pathobiochemistry, 
      Goethe-University Frankfurt, Frankfurt, Germany. bruene@pathobiochemie1.de
FAU - Dehne, Nathalie
AU  - Dehne N
FAU - Grossmann, Nina
AU  - Grossmann N
FAU - Jung, Michaela
AU  - Jung M
FAU - Namgaladze, Dmitry
AU  - Namgaladze D
FAU - Schmid, Tobias
AU  - Schmid T
FAU - von Knethen, Andreas
AU  - von Knethen A
FAU - Weigert, Andreas
AU  - Weigert A
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
DEP - 20130306
PL  - United States
TA  - Antioxid Redox Signal
JT  - Antioxidants & redox signaling
JID - 100888899
RN  - 0 (Inflammation Mediators)
RN  - 0 (Reactive Nitrogen Species)
RN  - 0 (Reactive Oxygen Species)
SB  - IM
MH  - Animals
MH  - Cell Hypoxia
MH  - Humans
MH  - Inflammation/*metabolism
MH  - Inflammation Mediators/physiology
MH  - *Macrophage Activation
MH  - Macrophages/immunology/*metabolism
MH  - Oxidation-Reduction
MH  - Oxidative Stress
MH  - Reactive Nitrogen Species/metabolism
MH  - Reactive Oxygen Species/metabolism
MH  - Signal Transduction
PMC - PMC3718318
EDAT- 2013/01/15 06:00
MHDA- 2014/02/04 06:00
PMCR- 2014/08/20
CRDT- 2013/01/15 06:00
PHST- 2013/01/15 06:00 [entrez]
PHST- 2013/01/15 06:00 [pubmed]
PHST- 2014/02/04 06:00 [medline]
PHST- 2014/08/20 00:00 [pmc-release]
AID - 10.1089/ars.2012.4785 [pii]
AID - 10.1089/ars.2012.4785 [doi]
PST - ppublish
SO  - Antioxid Redox Signal. 2013 Aug 20;19(6):595-637. doi: 10.1089/ars.2012.4785. 
      Epub 2013 Mar 6.