Evidence map›Paper›PMID 25028602›Full record

ArticleOxidative medicine and cellular longevity2014

Antioxidant supplement inhibits skeletal muscle constitutive autophagy rather than fasting-induced autophagy in mice.

Zhengtang Qi, Qiang He, Liu Ji, Shuzhe Ding

Open access · hybridAbstract read
In one paragraph

Article in Oxidative medicine and cellular longevity, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
2.4field-weighted citation impact, top 12% 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

10 citing papers in PubMed, 25 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Autophagy-Dependent Beneficial Effects of Exercise.Cold Spring Harbor perspectives in medicine · 2017
    Review
  7. PGC-1Physiological reports · 2017
    Article
  8. Redox regulation of autophagy in skeletal muscle.Free radical biology & medicine · 2016
    Review
  9. Article
  10. 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

4 authors at 1 institution in 1 country.

Zhengtang QiKey Laboratory of Adolescent Health Assessment and Exercise Intervention, Ministry of Education, East China Normal University, Shanghai 200241, China ; College of Physical Education and Health, East China Normal University, Shanghai 200241, China.
Qiang HeKey Laboratory of Adolescent Health Assessment and Exercise Intervention, Ministry of Education, East China Normal University, Shanghai 200241, China ; College of Physical Education and Health, East China Normal University, Shanghai 200241, China.
Liu JiKey Laboratory of Adolescent Health Assessment and Exercise Intervention, Ministry of Education, East China Normal University, Shanghai 200241, China ; College of Physical Education and Health, East China Normal University, Shanghai 200241, China.
Shuzhe DingKey Laboratory of Adolescent Health Assessment and Exercise Intervention, Ministry of Education, East China Normal University, Shanghai 200241, China ; College of Physical Education and Health, East China Normal University, Shanghai 200241, China.
East China Normal University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In this study, we tested the hypothesis that NAC administration leads to reduced oxidative stress and thus to decreased expression of autophagy markers in young mice. Our results reveal that NAC administration results in reduced muscle mRNA levels of several autophagy markers, including Beclin-1, Atg7, LC3, Atg9, and LAMP2. However, NAC supplement fails to block the activation of skeletal muscle autophagy in response to fasting, because fasting significantly increases the mRNA level of several autophagy markers and LC3 lipidation. We further examined the effects of NAC administration on mitochondrial antioxidant capacity in fed and 24-hour fasted mice. Our results clearly show that NAC administration depresses the expression of manganese superoxide dismutase (MnSOD) and TP53-induced glycolysis and apoptosis regulator (TIGAR), both of which play a predominant antioxidant role in mitochondria by reducing ROS level. In addition, we found no beneficial effect of NAC supplement on muscle mass but it can protect from muscle loss in response to fasting. Collectively, our findings indicate that ROS is required for skeletal muscle constitutive autophagy, rather than starvation-induced autophagy, and that antioxidant NAC inhibits constitutive autophagy by the regulation of mitochondrial ROS production and antioxidant capacity.

Indexed as

Dietary SupplementsAcetylcysteineAnimalsAntioxidantsApoptosis Regulatory ProteinsAutophagyBiomarkersDown-RegulationFastingGlycogenLipid PeroxidationMaleMice, Inbred ICRMicrotubule-Associated ProteinsMitochondriaMuscle, SkeletalAcetylcysteineAntioxidantsApoptosis Regulatory ProteinsBiomarkersGlycogenMap1lc3b protein, mouseMicrotubule-Associated ProteinsPhosphoric Monoester HydrolasesProteinsReactive Oxygen SpeciesSuperoxide DismutaseTIGAR protein, mouse

Identifiers

PMID25028602
PMCPMC4084590
OpenAlexW2110573505

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.