PMID- 12871043
OWN - NLM
STAT- MEDLINE
DCOM- 20040505
LR  - 20191107
IS  - 1568-0061 (Print)
IS  - 1568-0061 (Linking)
VI  - 3
IP  - 3
DP  - 2003 Sep
TI  - Hypoxia-inducible factor-1: a molecular hint of physiological changes in the 
      carotid body during long-term hypoxemia?
PG  - 254-9
AB  - The aims of this review are to describe recent data focusing on the anatomical, 
      functional and molecular changes of the carotid body during chronic hypoxemia, 
      and to summarize current views in the literature relevant to the topic. The 
      carotid body is the major peripheral sensor for detecting chemicals in the 
      arterial blood. In acute hypoxia, carotid chemoreceptors transduce the signal to 
      the brain for triggering reflexive responses of the cardiopulmonary system. The 
      carotid body enlarges and changes its hypoxic sensitivity in humans and animals 
      living at high altitude or subject to long-term hypoxemia associated with chronic 
      cardiopulmonary diseases or hematological disorders. Recently, a surge of new 
      evidence suggests that a heterodimeric transcriptional factor directly induced by 
      severe tissue or cellular hypoxia, namely hypoxia-inducible factor-1 (HIF-1), is 
      a key controller for the transcriptional regulation of the gene expression of a 
      spectrum of proteins for the cellular response to hypoxia. These proteins, such 
      as endothelin-1, type II nitric oxide synthase and vascular endothelial growth 
      factor, play important physiological roles in the control of vascular tone and 
      angiogenesis. In the carotid body, chronic hypoxemia induces remodeling of the 
      vasculature, stimulates proliferation of the chemosensitive cells, and changes 
      their excitability and sensitivity to chemical signals. In addition, 
      HIF-1-targeted genes are expressed in the carotid body and the expression is 
      modulated by chronic hypoxemia, suggesting an active role for HIF-1 in moderate 
      levels of hypoxic stress.
FAU - Fung, Man-Lung
AU  - Fung ML
AD  - Department of Physiology and Institute of Cardiovascular Science and Medicine, 
      Faculty of Medicine, University of Hong Kong, Hong Kong, China. 
      fungml@hkucc.hku.hk
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
PL  - Netherlands
TA  - Curr Drug Targets Cardiovasc Haematol Disord
JT  - Current drug targets. Cardiovascular & haematological disorders
JID - 101123341
RN  - 0 (DNA-Binding Proteins)
RN  - 0 (Endothelin-1)
RN  - 0 (HIF1A protein, human)
RN  - 0 (Hypoxia-Inducible Factor 1)
RN  - 0 (Hypoxia-Inducible Factor 1, alpha Subunit)
RN  - 0 (Nuclear Proteins)
RN  - 0 (Receptors, Endothelin)
RN  - 0 (Transcription Factors)
RN  - 0 (Vascular Endothelial Growth Factor A)
RN  - 31C4KY9ESH (Nitric Oxide)
RN  - EC 1.14.13.39 (Nitric Oxide Synthase)
RN  - EC 2.7.10.1 (Receptors, Vascular Endothelial Growth Factor)
SB  - IM
MH  - Animals
MH  - Carotid Body/*metabolism/pathology/*physiopathology
MH  - Chronic Disease
MH  - DNA-Binding Proteins/*metabolism
MH  - Endothelin-1/metabolism
MH  - Humans
MH  - Hypoxia/*metabolism
MH  - Hypoxia-Inducible Factor 1
MH  - Hypoxia-Inducible Factor 1, alpha Subunit
MH  - Nitric Oxide/biosynthesis
MH  - Nitric Oxide Synthase/biosynthesis
MH  - Nuclear Proteins/*metabolism
MH  - Receptors, Endothelin/metabolism
MH  - Receptors, Vascular Endothelial Growth Factor/metabolism
MH  - *Transcription Factors
MH  - Vascular Endothelial Growth Factor A/metabolism
RF  - 68
EDAT- 2003/07/23 05:00
MHDA- 2004/05/07 05:00
CRDT- 2003/07/23 05:00
PHST- 2003/07/23 05:00 [pubmed]
PHST- 2004/05/07 05:00 [medline]
PHST- 2003/07/23 05:00 [entrez]
AID - 10.2174/1568006033481447 [doi]
PST - ppublish
SO  - Curr Drug Targets Cardiovasc Haematol Disord. 2003 Sep;3(3):254-9. doi: 
      10.2174/1568006033481447.