Evidence map›Paper›PMID 18359899›Full record

ArticleAmerican journal of physiology. Heart and circulatory physiology2008

NFATc3 is required for intermittent hypoxia-induced hypertension.

Sergio de Frutos, Laura Duling, Dominique Alò, Tammy Berry, Olan Jackson-Weaver, Mary Walker, Nancy Kanagy, Laura González Bosc

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Heart and circulatory physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

26 citing papers in PubMed, 42 citations in OpenAlex.

  1. Article
  2. Article
  3. Simulated sleep apnea alters hydrogen sulfide regulation of blood flow and pressure.American journal of physiology. Heart and circulatory physiology · 2021
    Article
  4. Article
  5. PLCγ1-PKCε-IPAmerican journal of physiology. Lung cellular and molecular physiology · 2018
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. NFAT is required for spontaneous pulmonary hypertension in superoxide dismutase 1 knockout mice.American journal of physiology. Lung cellular and molecular physiology · 2013
    Article
  16. Preproendothelin-1 expression is negatively regulated by IFNγ during hepatic stellate cell activation.American journal of physiology. Gastrointestinal and liver physiology · 2012
    Article
  17. Review
  18. NFATc3 is required for chronic hypoxia-induced pulmonary hypertension in adult and neonatal mice.American journal of physiology. Lung cellular and molecular physiology · 2011
    Article
  19. Article
  20. 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

8 authors at 1 institution in 1 country.

Sergio de FrutosDepartment of Cell Biology and Physiology, School of Medicine, University of New Mexico, Albuquerque, NM 87131, USA.
Laura Duling
Dominique Alò
Tammy Berry
Olan Jackson-Weaver
Mary Walker
Nancy Kanagy
Laura González Bosc
University of New Mexico · US

Funding

NFATc3 in chronic hypoxic pulmonary hypertensionR01HL088151 · NHLBI · UNIVERSITY OF NEW MEXICO · PI GONZALEZ BOSC, LAURA V · 2008 to 2012
$2.0M
Endothelin vasoconstriction in a rat model of sleep apnea-induced hypertension.R01HL082799 · NHLBI · UNIVERSITY OF NEW MEXICO · PI KANAGY, NANCY L · 2007 to 2010
$1.5M
NHLBI NIH HHS R01 HL082799NHLBI NIH HHS R01 HL088151
6 · The paper itself

Abstract

Sleep apnea, defined as intermittent respiratory arrest during sleep, is associated with increased incidence of hypertension and peripheral vascular disease. Exposure of rodents to brief periods of intermittent hypercarbia/hypoxia (H-IH) during sleep mimics the cyclical hypoxia-normoxia of sleep apnea. Endothelin-1, an upstream activator of nuclear factor of activated T cells (NFAT), is increased during H-IH. Therefore, we hypothesized that NFATc3 is activated by H-IH and is required for H-IH-induced hypertension. Consistent with this hypothesis, we found that H-IH (20 brief exposures per hour to 5% O(2)-5% CO(2) for 7 h/day) induces systemic hypertension in mice [mean arterial pressure (MAP) = 97 +/- 2 vs. 124 +/- 2 mmHg, P < 0.05, n = 5] and increases NFATc3 transcriptional activity in aorta and mesenteric arteries. Cyclosporin A, an NFAT inhibitor, and genetic ablation of NFATc3 [NFATc3 knockout (KO)] prevented NFAT activation. More importantly, H-IH-induced hypertension was attenuated in cyclosporin A-treated mice and prevented in NFATc3 KO mice. MAP was significantly elevated in wild-type mice (Delta = 23.5 +/- 6.1 mmHg), but not in KO mice (Delta = -3.9 +/- 5.7). These results indicate that H-IH-induced increases in MAP require NFATc3 and that NFATc3 may contribute to the vascular changes associated with H-IH-induced hypertension.

Indexed as

Blood PressureAnimalsAortaCalcineurinCalcineurin InhibitorsCyclosporineDisease Models, AnimalEndothelin-1HypertensionHypoxiaLungMaleMesenteric ArteriesMiceMice, Inbred BALB CMice, KnockoutCalcineurinCalcineurin InhibitorsCyclosporineEndothelin-1Nfatc3 protein, mouseNFATC Transcription FactorsRNA, Messenger

Identifiers

PMID18359899
PMCPMC2953847
OpenAlexW2159590138

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.