Evidence map›Paper›PMID 32452827›Full record

ArticleAging2020

Regulation of PGC-1α mediated by acetylation and phosphorylation in MPP+ induced cell model of Parkinson's disease.

Fei Fan, Songlin Li, Zhipeng Wen, Qiaoyue Ye, Xiaochun Chen, Qinyong Ye

Open access · greenAbstract read
In one paragraph

Article in Aging, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

13 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Review
  6. Article
  7. Article
  8. Elucidating the Beneficial Effects of Ginger (ACS pharmacology & translational science · 2022
    Review
  9. Dioscin-Mediated Autophagy Alleviates MPPMolecules (Basel, Switzerland) · 2022
    Article
  10. Review
  11. CREB1ACS omega · 2021
    Article
  12. The Ageing Brain: Molecular and Cellular Basis of Neurodegeneration.Frontiers in cell and developmental biology · 2021
    Review
  13. 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

6 authors at 4 institutions in 1 country.

Fei FanDepartment of Neurology, Fujian Institute of Geriatrics, Fujian Medical University Union Hospital, Fuzhou, Fujian, China.
Songlin LiDepartment of Neurology, Fujian Institute of Geriatrics, Fujian Medical University Union Hospital, Fuzhou, Fujian, China.
Zhipeng WenDepartment of Neurology, Fujian Institute of Geriatrics, Fujian Medical University Union Hospital, Fuzhou, Fujian, China.
Qiaoyue YeFuzhou No. 8 High School, Fuzhou, Fujian, China.
Xiaochun ChenDepartment of Neurology, Fujian Institute of Geriatrics, Fujian Medical University Union Hospital, Fuzhou, Fujian, China.
Qinyong YeDepartment of Neurology, Fujian Institute of Geriatrics, Fujian Medical University Union Hospital, Fuzhou, Fujian, China.
Union Hospital · CNEducation Department of Fujian Province · CNFujian Medical University · CNPutian University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundParkinson's disease (PD) is one of the most common neurodegenerative diseases with complex etiology in sporadic cases. Accumulating evidence suggests that oxidative stress and defects in mitochondrial dynamics are associated with the pathogenesis of PD. The oxidative stress and mitochondrial dynamics are regulated strictly by peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α). We investigated whether acetylation and phosphorylation of PGC-1α contribute to protecting neuronal cell against oxidative stress.

resultsWe found that acetylation and phosphorylation mediated the nuclear translocation of PGC-1α protects against oxidative damage. In contrast to the increased nuclear PGC-1α, the cytosolic PGC-1α was decreased upon inhibition of GCN5 acetyltransferase. Similarly to the inhibition of GCN5 acetyltransferase, the increased nuclear PGC-1α and the decreased cytosolic PGC-1α were observed upon p38MAPK and AMPK activation. Briefly, the significantly increased nuclear PGC-1α is regulated either by inhibiting the acetylation of PGC-1α or by the phosphorylating PGC-1α, which results in a reduction in ROS.

conclusionPGC-1α protects neuronal cells against MPP

methodsWith established the 1-methyl-4-phenylpyridinium (MPP

Indexed as

1-Methyl-4-phenylpyridiniumAcetylationAMP-Activated Protein Kinase KinasesBlotting, WesternCell LineCell SurvivalFlow CytometryHumansMAP Kinase Signaling SystemOxidative Stressp300-CBP-Associated Factorp300-CBP Transcription Factorsp38 Mitogen-Activated Protein KinasesParkinson DiseasePeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPhosphorylation1-Methyl-4-phenylpyridiniumAMP-Activated Protein Kinase Kinasesp300-CBP-Associated Factorp300-CBP Transcription Factorsp38 Mitogen-Activated Protein KinasesPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPPARGC1A protein, humanProtein KinasesReactive Oxygen SpeciesAMPKGCN5p38MAPKParkinson’s diseasePGC-1α

Identifiers

PMID32452827
PMCPMC7288924
OpenAlexW3029364508

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.