Evidence map›Paper›PMID 26770656›Full record

ArticleOxidative medicine and cellular longevity2016

Resveratrol Regulates Mitochondrial Biogenesis and Fission/Fusion to Attenuate Rotenone-Induced Neurotoxicity.

Kaige Peng, Yuan Tao, Jun Zhang, Jian Wang, Feng Ye, Guorong Dan, Yuanpeng Zhao, Ying Cai, Jiqing Zhao, Qiang Wu and 3 more

Open access · hybridAbstract read
In one paragraph

Article in Oxidative medicine and cellular longevity, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed, 1 pooled it
3.2field-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

62 citing papers in PubMed, 1 synthesis or guideline pooled it, 118 citations in OpenAlex.

  1. Pooled it
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  16. Mitochondria in health, disease, and aging.Physiological reviews · 2023
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2 more citing papers are in PubMed but not listed here.

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

13 authors at 1 institution in 1 country.

Kaige PengInstitute of Toxicology, College of Preventive Medicine, Third Military Medical University, Chongqing 400038, China.
Yuan TaoCollege of Preventive Medicine, Third Military Medical University, Chongqing 400038, China.
Jun ZhangCollege of Preventive Medicine, Third Military Medical University, Chongqing 400038, China.
Jian WangInstitute of Toxicology, College of Preventive Medicine, Third Military Medical University, Chongqing 400038, China.
Feng YeInstitute of Toxicology, College of Preventive Medicine, Third Military Medical University, Chongqing 400038, China.
Guorong DanInstitute of Toxicology, College of Preventive Medicine, Third Military Medical University, Chongqing 400038, China.
Yuanpeng ZhaoInstitute of Toxicology, College of Preventive Medicine, Third Military Medical University, Chongqing 400038, China.
Ying CaiInstitute of Toxicology, College of Preventive Medicine, Third Military Medical University, Chongqing 400038, China.
Jiqing ZhaoInstitute of Toxicology, College of Preventive Medicine, Third Military Medical University, Chongqing 400038, China.
Qiang WuCollege of Preventive Medicine, Third Military Medical University, Chongqing 400038, China.
Zhongmin ZouInstitute of Toxicology, College of Preventive Medicine, Third Military Medical University, Chongqing 400038, China.
Jia CaoInstitute of Toxicology, College of Preventive Medicine, Third Military Medical University, Chongqing 400038, China.
Yan SaiInstitute of Toxicology, College of Preventive Medicine, Third Military Medical University, Chongqing 400038, China.
Army Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

It has been confirmed that mitochondrial impairment may underlie both sporadic and familial Parkinson's disease (PD). Mitochondrial fission/fusion and biogenesis are key processes in regulating mitochondrial homeostasis. Therefore, we explored whether the protective effect of resveratrol in rotenone-induced neurotoxicity was associated with mitochondrial fission/fusion and biogenesis. The results showed that resveratrol could not only promote mitochondrial mass and DNA copy number but also improve mitochondrial homeostasis and neuron function in rats and PC12 cells damaged by rotenone. We also observed effects with alterations in proteins known to regulate mitochondrial fission/fusion and biogenesis in rotenone-induced neurotoxicity. Therefore, our findings suggest that resveratrol may prevent rotenone-induced neurotoxicity through regulating mitochondrial fission/fusion and biogenesis.

Indexed as

Organelle BiogenesisAdenosine TriphosphateAnimalsApoptosisCell ShapeCell SurvivalDNA, MitochondrialGene DosageMaleMitochondriaMitochondrial DynamicsMotor ActivityNeuroprotective AgentsNeurotoxinsPC12 CellsPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaAdenosine TriphosphateDNA, MitochondrialNeuroprotective AgentsNeurotoxinsPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPpargc1a protein, ratReactive Oxygen SpeciesResveratrolRotenoneStilbenesTranscription Factors

Identifiers

PMID26770656
PMCPMC4684867
OpenAlexW2100167021

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.