PMID- 25546605
OWN - NLM
STAT- MEDLINE
DCOM- 20151208
LR  - 20220316
IS  - 1097-4644 (Electronic)
IS  - 0730-2312 (Linking)
VI  - 116
IP  - 5
DP  - 2015 May
TI  - Regulation of hypoxia-inducible factor-1a by reactive oxygen species: new 
      developments in an old debate.
PG  - 696-703
LID - 10.1002/jcb.25074 [doi]
AB  - Hypoxia-Inducible Factor-1 (HIF-1) has been largely studied for its role in cell 
      survival in hypoxic conditions. The regulation of HIF-1 is a complex process and 
      involves a number of molecules and pathways. Among these mechanisms a direct 
      regulatory role of reactive oxygen species (ROS) on HIF-1 alpha subunit has 
      received a great deal of attention and the existing body of literature includes 
      many contradictory findings. Other intermediates such as nitric oxide (NO), 
      specific microRNAs (miR), and transcriptional and post-translational modification 
      have also been implicated as players in ROS mediated HIF-1a regulation. The focus 
      of this review is to present the past conflicting evidence along with more recent 
      findings in order to relate various aspects of this complex process. Aside from 
      the direct role of ROS on HIF-1a regulation under hypoxia and normoxia, we 
      analyzed the effect of different sources and concentrations of NO and the 
      interplay between superoxide (SO) and NO in this process. We also present 
      findings on transcriptional and translational regulation of HIF-1a via ROS and 
      the interplay with microRNAs in this process. This review further provides 
      insight on ERK and PI3K/AKT signaling as a common mechanism relating several 
      pathways of ROS mediated HIF-1a regulation. Ultimately further research and 
      discovery regarding HIF-1 regulation by oxidative stress is warranted for better 
      understanding of disease development and potential therapeutics for pathologies 
      such as cancer, inflammatory diseases, and ischemia-reperfusion injury.
CI  - (c) 2014 Wiley Periodicals, Inc.
FAU - Movafagh, Shahrzad
AU  - Movafagh S
AD  - Department of Pharmacogenomics, Bernard J. Dunn School of Pharmacy, Shenandoah 
      University, Ashburn, Virginia.
FAU - Crook, Sean
AU  - Crook S
FAU - Vo, Kim
AU  - Vo K
LA  - eng
PT  - Journal Article
PT  - Review
PL  - United States
TA  - J Cell Biochem
JT  - Journal of cellular biochemistry
JID - 8205768
RN  - 0 (Hypoxia-Inducible Factor 1, alpha Subunit)
RN  - 0 (MicroRNAs)
RN  - 0 (Reactive Oxygen Species)
RN  - 11062-77-4 (Superoxides)
RN  - 31C4KY9ESH (Nitric Oxide)
RN  - EC 2.7.1.- (Phosphatidylinositol 3-Kinases)
RN  - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
SB  - IM
MH  - Cell Hypoxia
MH  - Humans
MH  - Hypoxia-Inducible Factor 1, alpha Subunit/genetics/*metabolism
MH  - MAP Kinase Signaling System
MH  - MicroRNAs/metabolism
MH  - Mitochondria/metabolism
MH  - Nitric Oxide/metabolism
MH  - Phosphatidylinositol 3-Kinases/metabolism
MH  - Proto-Oncogene Proteins c-akt/metabolism
MH  - Reactive Oxygen Species/*metabolism
MH  - Signal Transduction
MH  - Superoxides/metabolism
OTO - NOTNLM
OT  - ERK
OT  - HIF-1
OT  - HYPOXIA
OT  - MICRORNA
OT  - NITRIC OXIDE
OT  - PI3K/AKT
OT  - SUPEROXIDE
EDAT- 2014/12/30 06:00
MHDA- 2015/12/15 06:00
CRDT- 2014/12/30 06:00
PHST- 2014/12/17 00:00 [received]
PHST- 2014/12/18 00:00 [accepted]
PHST- 2014/12/30 06:00 [entrez]
PHST- 2014/12/30 06:00 [pubmed]
PHST- 2015/12/15 06:00 [medline]
AID - 10.1002/jcb.25074 [doi]
PST - ppublish
SO  - J Cell Biochem. 2015 May;116(5):696-703. doi: 10.1002/jcb.25074.