Evidence map›Paper›PMID 27060608›Full record

ReviewThe Journal of physiology2016

Mitochondria in the middle: exercise preconditioning protection of striated muscle.

John M Lawler, Dinah A Rodriguez, Jeffrey M Hord

Open access · greenAbstract readReview
In one paragraph

Review in The Journal of physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 1 pooled it
6.8field-weighted citation impact, top 3% 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

28 citing papers in PubMed, 1 synthesis or guideline pooled it, 54 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Review
  11. Review
  12. Article
  13. The mechanism and prevention of mitochondrial injury after exercise.Journal of physiology and biochemistry · 2021
    Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Review
  19. Article
  20. Nanoparticle Exposure and Hormetic Dose-Responses: An Update.International journal of molecular sciences · 2018
    Review
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

3 authors at 1 institution in 1 country.

John M LawlerRedox Biology & Cell Signalling Laboratory, Department of Health and Kinesiology, Graduate Faculty of Nutrition & Food Science, Texas A&M University, College Station, TX, USA. jml2621@email.tamu.edu.ORCID 0000-0001-8055-7703
Dinah A RodriguezRedox Biology & Cell Signalling Laboratory, Department of Health and Kinesiology, Graduate Faculty of Nutrition & Food Science, Texas A&M University, College Station, TX, USA.
Jeffrey M HordRedox Biology & Cell Signalling Laboratory, Department of Health and Kinesiology, Graduate Faculty of Nutrition & Food Science, Texas A&M University, College Station, TX, USA.
Texas A&M University System · US

Funding

Regulation of Oxidative Stress in the mdx DiaphragmR03AR054084 · NIAMS · TEXAS A&M UNIVERSITY · PI LAWLER, JOHN M · 2006 to 2008
$204k
NIAMS NIH HHS R03 AR054084
6 · The paper itself

Abstract

Cellular and physiological adaptations to an atmosphere which became enriched in molecular oxygen spurred the development of a layered system of stress protection, including antioxidant and stress response proteins. At physiological levels reactive oxygen and nitrogen species regulate cell signalling as well as intracellular and intercellular communication. Exercise and physical activity confer a variety of stressors on skeletal muscle and the cardiovascular system: mechanical, metabolic, oxidative. Transient increases of stressors during acute bouts of exercise or exercise training stimulate enhancement of cellular stress protection against future insults of oxidative, metabolic and mechanical stressors that could induce injury or disease. This phenomenon has been termed both hormesis and exercise preconditioning (EPC). EPC stimulates transcription factors such as Nrf-1 and heat shock factor-1 and up-regulates gene expression of a cadre of cytosolic (e.g. glutathione peroxidase and heat shock proteins) and mitochondrial adaptive or stress proteins (e.g. manganese superoxide dismutase, mitochondrial KATP channels and peroxisome proliferator activated receptor γ coactivator-1 (PGC-1)). Stress response and antioxidant enzyme inducibility with exercise lead to protection against striated muscle damage, oxidative stress and injury. EPC may indeed provide significant clinical protection against ischaemia-reperfusion injury, Type II diabetes and ageing. New molecular mechanisms of protection, such as δ-opioid receptor regulation and mitophagy, reinforce the notion that mitochondrial adaptations (e.g. heat shock proteins, antioxidant enzymes and sirtuin-1/PGC-1 signalling) are central to the protective effects of exercise preconditioning.

Indexed as

AnimalsExerciseHumansMitochondriaMuscle, StriatedOxidative Stress

Identifiers

PMID27060608
PMCPMC5023703
OpenAlexW2319713015

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.