Evidence map›Paper›PMID 23459758›Full record

ReviewThe Journal of physiology2013

Sensing hypoxia: physiology, genetics and epigenetics.

Nanduri R Prabhakar

Open access · greenAbstract readReview
In one paragraph

Review in The Journal of physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers.

0numbers the graph read from it
0cells of the map it votes in
76citing papers in PubMed
9.3field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

76 citing papers in PubMed, 138 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Carotid body responses to OActa physiologica (Oxford, England) · 2022
    Article
  13. Obstructive sleep apnea.Handbook of clinical neurology · 2022
    Review
  14. Review
  15. Review
  16. Review
  17. Review
  18. Article
  19. Hypoxia-inducible factors and obstructive sleep apnea.The Journal of clinical investigation · 2020
    Review
  20. Neuronal Networks in Hypertension: Recent Advances.Hypertension (Dallas, Tex. : 1979) · 2020
    Review

16 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

1 author at 1 institution in 1 country.

Nanduri R PrabhakarInstitute for Integrative Physiology, Center for Systems Biology of O(2) Sensing, Biological Sciences Division, University of Chicago, Chicago, IL 60637, USA. nanduri@uchicago.edu
University of Chicago · US

Funding

Integrative Consequences of HypoxiaP01HL090554 · NHLBI · UNIVERSITY OF CHICAGO · PI PRABHAKAR, NANDURI R · 2008 to 2017
$21.4M
Consequences of Neonatal HypoxiaR01HL076537 · NHLBI · UNIVERSITY OF CHICAGO · PI PRABHAKAR, NANDURI R · 2005 to 2009
$1.8M
Transmitters in Altered Carotid Body FunctionR01HL086493 · NHLBI · UNIVERSITY OF CHICAGO · PI PRABHAKAR, NANDURI R · 2008 to 2012
$1.8M
NHLBI NIH HHS P01 HL090554NHLBI NIH HHS P01-HL90554NHLBI NIH HHS R01 HL076537NHLBI NIH HHS R01 HL086493NHLBI NIH HHS R01-HL76537NHLBI NIH HHS R01-HL86493
6 · The paper itself

Abstract

The carotid body is a sensory organ for detecting arterial blood O2 levels and reflexly mediates systemic cardiac, vascular and respiratory responses to hypoxia. This article presents a brief review of the roles of gaseous messengers in the sensory transduction at the carotid body, genetic and epigenetic influences on hypoxic sensing and the role of the carotid body chemoreflex in cardiorespiratory diseases. Type I (also called glomus) cells, the site of O2 sensing in the carotid body, express haem oxygenase-2 and cystathionine-γ-lyase, the enzymes which catalyse the generation of CO and H2S, respectively. Physiological studies have shown that CO is an inhibitory gas messenger, which contributes to the low sensory activity during normoxia, whereas H2S is excitatory and mediates sensory stimulation by hypoxia. Hypoxia-evoked H2S generation in the carotid body requires the interaction of cystathionine-γ-lyase with haem oxygenase-2, which generates CO. Hypoxia-inducible factors 1 and 2 constitute important components of the genetic make-up in the carotid body, which influence hypoxic sensing by regulating the intracellular redox state via transcriptional regulation of pro- and antioxidant enzymes. Recent studies suggest that developmental programming of the carotid body response to hypoxia involves epigenetic changes, e.g. DNA methylation of genes encoding redox-regulating enzymes. Emerging evidence implicates heightened carotid body chemoreflex in the progression of autonomic morbidities associated with cardiorespiratory diseases, such as sleep-disordered breathing with apnoea, congestive heart failure and essential hypertension.

Indexed as

AnimalsCarbon MonoxideCarotid BodyEpigenesis, GeneticHumansHydrogen SulfideHypoxiaCarbon MonoxideHydrogen Sulfide

Identifiers

PMID23459758
PMCPMC3650692
OpenAlexW1521217781

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.