Evidence map›Paper›PMID 22349394›Full record

ReviewJournal of molecular medicine (Berlin, Germany)2012

Gaseous messengers in oxygen sensing.

Nanduri R Prabhakar, Gregg L Semenza

Abstract readReview
PubMed Publisher
In one paragraph

Review in Journal of molecular medicine (Berlin, Germany), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
4.1field-weighted citation impact, top 5% 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

40 citing papers in PubMed, 71 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Article
  6. Carotid Body Dysfunction and Mechanisms of Disease.Advances in anatomy, embryology, and cell biology · 2023
    Article
  7. Neurochemical Anatomy of the Mammalian Carotid Body.Advances in anatomy, embryology, and cell biology · 2023
    Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Epigenetic changes by DNA methylation in chronic and intermittent hypoxia.American journal of physiology. Lung cellular and molecular physiology · 2017
    Review
  18. Systems biology of oxygen homeostasis.Wiley interdisciplinary reviews. Systems biology and medicine · 2017
    Review
  19. Article
  20. Ganglionic GFAPJCI insight · 2017
    Article
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

2 authors at 2 institutions in 1 country.

Nanduri R PrabhakarInstitute for Integrative Physiology and Center for Systems Biology of O2 Sensing, The University of Chicago, Chicago, IL 60637, USA. nanduri@uchicago.edu
Gregg L Semenza
Johns Hopkins Medicine · USUniversity 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 HL-76537NHLBI NIH HHS HL-86493NHLBI NIH HHS HL-90554
6 · The paper itself

Abstract

The carotid body is a sensory organ that detects acute changes in arterial blood oxygen (O(2)) levels and reflexly mediates systemic cardiac, vascular, and respiratory responses to hypoxia. This article provides a brief update of the roles of gas messengers as well as redox homeostasis by hypoxia-inducible factors (HIFs) in hypoxic sensing by the carotid body. Carbon monoxide (CO) and nitric oxide (NO), generated by heme oxygenase-2 (HO-2) and neuronal nitric oxide synthase (nNOS), respectively, inhibit carotid body activity. Molecular O(2) is a required substrate for the enzymatic activities of HO-2 and nNOS. Stimulation of carotid body activity by hypoxia may reflect reduced formation of CO and NO. Glomus cells, the site of O(2) sensing in the carotid body, express cystathionine γ-lyase (CSE), an H(2)S generating enzyme. Cth ( -/- ) mice, which lack CSE, exhibit severely impaired hypoxia-induced H(2)S generation, sensory excitation, and stimulation of breathing in response to low O(2). Hypoxia-evoked H(2)S generation in the carotid body requires the interaction of CSE with HO-2, which generates CO. Carotid bodies from Hif1a ( +/- ) mice with partial HIF-1α deficiency do not respond to hypoxia, whereas carotid bodies from mice with partial HIF-2α deficiency are hyper-responsive to hypoxia. The opposing roles of HIF-1α and HIF-2α in the carotid body have provided novel insight into molecular mechanisms of redox homeostasis and its role in hypoxia sensing. Heightened carotid body activity has been implicated in the pathogenesis of autonomic morbidities associated with sleep-disordered breathing, congestive heart failure, and essential hypertension. The enzymes that generate gas messengers and redox regulation by HIFs represent potential therapeutic targets for normalizing carotid body function and downstream autonomic output in these disease states.

Indexed as

AnimalsCarbon MonoxideCarotid BodyGasesHumansHydrogen SulfideHypoxiaMiceNitric OxideOxygenReactive Oxygen SpeciesSecond Messenger SystemsCarbon MonoxideGasesHydrogen SulfideNitric OxideOxygenReactive Oxygen Species

Identifiers

PMID22349394
OpenAlexW2088239014

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.