Evidence map›Paper›PMID 24590457›Full record

ArticleCell stress & chaperones2014

Differential hypoxic tolerance is mediated by activation of heat shock response and nitric oxide pathway.

Kanika Jain, Geetha Suryakumar, Lilly Ganju, Shashi Bala Singh

Open access · bronzeAbstract read
In one paragraph

Article in Cell stress & chaperones, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.4field-weighted citation impact, top 17% 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

23 citing papers in PubMed, 43 citations in OpenAlex.

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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

4 authors at 1 institution in 1 country.

Kanika JainCellular Biochemistry Division, Defence Institute of Physiology and Allied Sciences, Lucknow Road, Timarpur, Delhi, 110054, India.
Geetha Suryakumar
Lilly Ganju
Shashi Bala Singh
Defence Institute of Physiology and Allied Sciences · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The fall in ambient oxygen pressure in high-altitude milieu elicits a wide range of physiological responses in the myocardium, which may differ from individual to individual. This condition, known as hypobaric hypoxia, invokes the cardioprotective heat shock response. The present study focuses on the role played by this ubiquitous response in mediating a differential tolerance to acute hypoxic stress. Sprague Dawley rats were exposed to simulated hypoxia equivalent to 223 mmHg pressure, screened on the basis of time taken for onset of a characteristic hyperventilatory response, and categorized as susceptible (<10 min), normal (10-25 min), or tolerant (>25 min). The tolerant animals displayed a significant upregulation of heat shock protein (Hsp)70/HSPA, evident through immunohistochemical staining of the cardiac tissue. The increased expression of transcription factor heat shock factor-1 led to the downstream activation of other chaperones, including Hsp90/HSPC, Hsp60/HSPD1, and Hsp27/HSPB1. The higher induction of HSPs in tolerant animals contributed to higher nitric oxide synthesis mediated by both endothelial nitric oxide synthase and inducible nitric oxide synthase activation. Conversely, susceptible animals showed significantly higher expression of the proinflammatory markers tumor necrosis factor alpha and nuclear factor kappa-light-chain enhancer of activated B cells in the myocardium. Evaluation of circulatory stress markers identified increased levels of reactive oxygen species, corticosterone and endothelin-1 in the susceptible animals highlighting their vulnerability to hypoxic stress. The heat shock response, through the action of chaperones and enhanced NO generation thus contributes substantially to the ability to sustain survival under acute sub lethal hypoxia.

Indexed as

AcclimatizationHeat-Shock ResponseAltitudeAnimalsDisease Models, AnimalEnzyme ActivationHeat-Shock ProteinsHypoxiaInflammation MediatorsLungMaleMyocardiumNitric OxideNitric Oxide Synthase Type IINitric Oxide Synthase Type IIIPulmonary VentilationHeat-Shock ProteinsInflammation MediatorsNitric OxideNitric Oxide Synthase Type IINitric Oxide Synthase Type IIINos2 protein, ratNos3 protein, rat

Identifiers

PMID24590457
PMCPMC4389840
OpenAlexW2011674227

What OpenQuestion holds

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Registered trials

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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.