Evidence map›Paper›PMID 27747840›Full record

ArticleSports medicine - open2015

A tutorial on oxidative stress and redox signaling with application to exercise and sedentariness.

Robert Buresh, Kris Berg

Open access · goldAbstract read
In one paragraph

Article in Sports medicine - open, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
3.6field-weighted citation impact, top 8% 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

8 citing papers in PubMed, 20 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

2 authors at 2 institutions in 1 country.

Robert BureshDepartment of Exercise Science and Sport Management, Kennesaw State University, 520 Parliament Garden Way NW, Kennesaw, GA, 30144, USA. rburesh@kennesaw.edu.
Kris BergSchool of Health, Physical Education, and Recreation, University of Nebraska at Omaha, Omaha, NE, USA.
Kennesaw State University · USUniversity of Nebraska at Omaha · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Oxidative stress has been shown to play a role in the etiology of several chronic diseases, including cardiovascular disease, diabetes mellitus, and cancer. Free radicals and, most prominently, the superoxide radical, result from oxidative metabolism and several enzyme-catalyzed reactions, and endogenous cellular antioxidants dismutate many reactive oxygen species (ROS). Under certain conditions, ROS production can outpace dismutation (e.g., long-term sedentariness and positive energy balance) and the result is oxidative stress, with proteins, lipids, and DNA the most common targets of radicals. However, the molecules that contribute to oxidative stress also appear to participate in vital cell signaling activity that supports health and stimulates favorable adaptations to exercise training, such that inhibiting ROS formation prevents common adaptations to training. Furthermore, researchers have recently suggested that some proteins are not as readily formed when the redox state of the cell is insufficiently oxidative. Exercise training appears to optimize the redox environment by dramatically enhancing the capacity of the cell to neutralize ROS while regularly creating oxidative environments in which membrane and secretory proteins can be synthesized. The role that exercise plays in enhancing management of ROS likely explains many of the associated health benefits.

Identifiers

PMID27747840
PMCPMC4532704
OpenAlexW2111061453

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.