Evidence map›Paper›PMID 22187044›Full record

ArticleHistochemistry and cell biology2012

Chronic intermittent hypoxia induces local inflammation of the rat carotid body via functional upregulation of proinflammatory cytokine pathways.

Siu-Yin Lam, Yu Liu, Kwong-Man Ng, Chi-Fai Lau, Emily C Liong, George L Tipoe, Man-Lung Fung

Open access · hybridAbstract read
In one paragraph

Article in Histochemistry and cell biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

62 citing papers in PubMed, 105 citations in OpenAlex.

  1. Trial
  2. Review
  3. Review
  4. Review
  5. Article
  6. Article
  7. Chronic intermittent hypoxia-induced hypertension: the impact of sex hormones.American journal of physiology. Regulatory, integrative and comparative physiology · 2024
    Review
  8. Review
  9. Review
  10. Carotid Body Dysfunction and Mechanisms of Disease.Advances in anatomy, embryology, and cell biology · 2023
    Article
  11. Neurochemical Plasticity of the Carotid Body.Advances in anatomy, embryology, and cell biology · 2023
    Article
  12. Review
  13. Article
  14. Review
  15. Review
  16. Review
  17. Article
  18. Review
  19. Article
  20. Review

2 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

7 authors at 1 institution in 1 country.

Siu-Yin LamDepartment of Physiology, University of Hong Kong, Pokfulam, Hong Kong, China.
Yu Liu
Kwong-Man Ng
Chi-Fai Lau
Emily C Liong
George L Tipoe
Man-Lung Fung
University of Hong Kong · HK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Maladaptive changes in the carotid body (CB) induced by chronic intermittent hypoxia (IH) account for the pathogenesis of cardiovascular morbidity in patients with sleep-disordered breathing. We postulated that the proinflammatory cytokines, namely interleukin (IL)-1β, IL-6 and tumor necrosis factor (TNF)-α, and cytokine receptors (IL-1r1, gp130 and TNFr1) locally expressed in the rat CB play a pathophysiological role in IH-induced CB inflammation. Results showed increased levels of oxidative stress (serum 8-isoprostane and nitrotyrosine in the CB) in rats with 7-day IH treatment resembling recurrent apneic conditions when compared with the normoxic control. Local inflammation shown by the amount of ED1-containing cells (macrophage infiltration) and the gene transcripts of NADPH oxidase subunits (gp91(phox) and p22(phox)) and chemokines (MCP-1, CCR2, MIP-1α, MIP-1β and ICAM-1) in the CB were significantly more in the hypoxic group than in the control. In addition, the cytokines and receptors were expressed in the lobules of chemosensitive glomus cells containing tyrosine hydroxylase and the levels of expressions were significantly increased in the hypoxic group. Exogenous cytokines elevated the intracellular calcium ([Ca(2+)](i)) response to acute hypoxia in the dissociated glomus cells. The effect of cytokines on the [Ca(2+)](i) response was significantly greater in the hypoxic than in the normoxic group. Moreover, daily treatment of IH rats with anti-inflammatory drugs (dexamethasone or ibuprofen) attenuated the levels of oxidative stress, gp91(phox) expression and macrophage infiltration in the CB. Collectively, these results suggest that the upregulated expression of proinflammatory cytokine pathways could mediate the local inflammation and functional alteration of the CB under chronic IH conditions.

Indexed as

AnimalsAnti-Inflammatory AgentsAnti-Inflammatory Agents, Non-SteroidalCalciumCarotid Artery, InternalCarotid BodyChronic DiseaseCytokinesDexamethasoneDisease Models, AnimalGene ExpressionHypoxiaIbuprofenMaleOxidative StressRatsAnti-Inflammatory AgentsAnti-Inflammatory Agents, Non-SteroidalCalciumCytokinesDexamethasoneIbuprofenReceptors, Cytokine

Identifiers

PMID22187044
PMCPMC3278607
OpenAlexW2082170144

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.