Evidence map›Paper›PMID 35345510›Full record

ArticleCurrent research in physiology2022

Developing chicken cardiac muscle mitochondria are resistant to variations in incubation oxygen levels.

Vanessa J Starr, Edward M Dzialowski

Open access · goldAbstract read
In one paragraph

Article in Current research in physiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.4field-weighted citation impact, top 42% 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

1 citing paper in PubMed, 5 citations in OpenAlex.

  1. 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 1 institution in 1 country.

Vanessa J StarrDevelopmental Integrative Biology, Department of Biological Sciences, 1155 Union Circle #305220, University of North Texas, Denton, TX, 76203, USA.
Edward M DzialowskiDevelopmental Integrative Biology, Department of Biological Sciences, 1155 Union Circle #305220, University of North Texas, Denton, TX, 76203, USA.
University of North Texas · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Chronic exposure to hypoxia during vertebrate development can produce abnormal cardiovascular morphology and function. The aim of this study was to examine cardiac mitochondria function in an avian model, the chicken, in response to embryonic development under hypoxic (15% O Methods: Chicken embryos were incubated in hypoxia, normoxia, or hyperoxia beginning on day 5 of incubation through hatching. Cardiac mitochondria oxygen flux and reactive oxygen species production were measured in permeabilized cardiac fibers from externally pipped and 1-day post hatchlings. Results: Altering oxygen during development had a large effect on body and heart masses of externally pipped embryos and 1-day old hatchlings. Hypoxic animals had smaller body masses and absolute heart masses, but proportionally similar sized hearts compared to normoxic animals during external pipping. Hyperoxic animals were larger with larger hearts than normoxic animals during external pipping. Mitochondrial oxygen flux in permeabilized cardiac muscle fibers revealed limited effects of developing under altered oxygen conditions, with only oxygen flux through cytochrome oxidase being lower in hypoxic hearts compared with hyperoxic hearts. Oxygen flux in leak and oxidative phosphorylation states were not affected by developmental oxygen levels. Mitochondrial reactive oxygen species production under leak and oxidative phosphorylation states studied did not differ between any developmental oxygen treatment. Conclusions: These results suggest that cardiac mitochondria function of the developing chicken is not altered by developing

Indexed as

AA, Antimycin AADP, adenosine diphosphateCardiac mitochondriaChickenCOX, cytochrome oxidasedph, days post hatchingEP, external pippingGMP, glutamate, malate, and pyruvateHyperoxiaHypoxiaIP, internal pippingLEAK, mitochondrial leak respirationOMY, oligomycinOXPHOS, mitochondrial oxidative phosphorylationReactive oxygen speciesROS, reactive oxygen speciesROT, rotenoneS, succinateTMPD, N,N,N’,N’-tetramethyl-p-phenylenediamine

Identifiers

PMID35345510
PMCPMC8956876
OpenAlexW4225962920

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.