Evidence map›Paper›PMID 30242625›Full record

ArticleNeurotoxicity research2019

Mutual Antagonism of PINK1/Parkin and PGC-1α Contributes to Maintenance of Mitochondrial Homeostasis in Rotenone-Induced Neurotoxicity.

Kaige Peng, Jingsong Xiao, Likui Yang, Feng Ye, Jia Cao, Yan Sai

Abstract read
PubMed Publisher
In one paragraph

Article in Neurotoxicity research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.9field-weighted citation impact, top 10% 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

23 citing papers in PubMed, 51 citations in OpenAlex.

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  14. Mitochondria in health, disease, and aging.Physiological reviews · 2023
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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

6 authors at 1 institution in 1 country.

Kaige PengInstitute of Toxicology, College of Preventive Medicine, Third Military Medical University, Chongqing, 400038, People's Republic of China.
Jingsong XiaoInstitute of Toxicology, College of Preventive Medicine, Third Military Medical University, Chongqing, 400038, People's Republic of China.
Likui YangInstitute of Toxicology, College of Preventive Medicine, Third Military Medical University, Chongqing, 400038, People's Republic of China.
Feng YeInstitute of Toxicology, College of Preventive Medicine, Third Military Medical University, Chongqing, 400038, People's Republic of China.
Jia CaoInstitute of Toxicology, College of Preventive Medicine, Third Military Medical University, Chongqing, 400038, People's Republic of China.
Yan SaiInstitute of Toxicology, College of Preventive Medicine, Third Military Medical University, Chongqing, 400038, People's Republic of China. sai2000cn@163.com.
Army Medical University · CN

Funding

National Natural Science Foundation of China 81273106National Natural Science Foundation of China 81473006
6 · The paper itself

Abstract

Parkinson's disease (PD) is a progressive, selective, and age-related neurodegenerative disease. The pathogenic focus of PD is mitochondrial dysfunction. When mitochondrial homeostasis was damaged, it can lead to reactive oxygen species formation to further accelerate the accumulation of dysfunctional mitochondria, resulting in a vicious cycle harmful to the neuron. PINK1 and Parkin, two proteins that are linked to PD, play vital roles in mitophagy, which was very important in maintaining mitochondrial homeostasis. Thus, at present, we explored mitochondrial biogenesis, mitophagy, and fission/fusion in rotenone-induced dopamine neurotoxicity. In particular, we focused on interactions between the PINK1/Parkin pathway and PGC-1α in the regulation of mitochondrial homeostasis impairment. The results indicated that both the autophagy and mitophagy levels increased significantly and were accompanied by altered levels of PINK1/Parkin proteins in rotenone-induced neurotoxicity. PINK1 influenced mitochondrial biogenesis by inhibiting PGC-1α and mtTFA protein expression as well as the mtDNA copy number. PGC-1α, in turn, inhibited PINK1/Parkin protein expression and the mitophagy levels. Furthermore, the results demonstrated that PINK1 influenced mitochondrial fission/fusion by regulating MFN2 and phosphorylating Drp1. In summary, mutual antagonism of the PINK1/Parkin pathway and PGC-1α formed a balance that regulated mitochondrial biogenesis, fission/fusion, and mitophagy. These effects contributed to the maintenance of mitochondrial homeostasis in rotenone-induced neurotoxicity.

Indexed as

Protein KinasesAnimalsCell SurvivalDose-Response Relationship, DrugHomeostasisMitochondriaPC12 CellsPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPTEN-Induced Putative KinaseRatsRotenoneUbiquitin-Protein Ligasesparkin proteinPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPpargc1a protein, ratProtein KinasesPTEN-Induced Putative KinaseRotenoneUbiquitin-Protein LigasesMitochondrial biogenesisMitochondrial fission/fusionMitophagyPGC-1αPINK1/ParkinRotenone

Identifiers

PMID30242625
OpenAlexW2889877280

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.