Evidence map›Paper›PMID 35039479›Full record

ArticleCell death discovery2022

Idebenone improves motor dysfunction, learning and memory by regulating mitophagy in MPTP-treated mice.

Junqiang Yan, Wenjie Sun, Mengmeng Shen, Yongjiang Zhang, Menghan Jiang, Anran Liu, Hongxia Ma, Xiaoyi Lai, Jiannan Wu

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell death discovery, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
5.1field-weighted citation impact, top 4% 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

29 citing papers in PubMed, 48 citations in OpenAlex.

  1. Review
  2. Article
  3. Idebenone in Rapid Eye Movement Sleep Behavioral Disorder for Parkinson's Disease Prevention.Movement disorders : official journal of the Movement Disorder Society · 2026
    Article
  4. Article
  5. Article
  6. The α-synuclein proteostasis network and its translational applications in Parkinson's disease.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  7. Article
  8. Dystonia: Insights into Mechanisms and Novel Therapeutics.Current neurology and neuroscience reports · 2026
    Review
  9. Review
  10. Review
  11. Neuroprotection in Parkinson Disease.Neurology and therapy · 2025
    Review
  12. Aryl hydrocarbon receptor (AhR) alleviates the LPS-induced inflammatory responses in IPEC-J2 cells by activating PINK1/Parkin-mediated mitophagy.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
    Article
  13. Review
  14. Review
  15. Review
  16. Review
  17. Central Role of Hypothalamic Circuits for Acupuncture's Anti-Parkinsonian Effects.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
    Article
  18. Review
  19. Article
  20. 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

9 authors at 1 institution in 1 country.

Junqiang YanNeuromolecular Biology Laboratory, The First Affiliated Hospital, and College of Clinical Medicine of Henan University of Science and Technology, Luoyang, 471003, China. yanjq@haust.edu.cn.
Wenjie SunNeuromolecular Biology Laboratory, The First Affiliated Hospital, and College of Clinical Medicine of Henan University of Science and Technology, Luoyang, 471003, China.
Mengmeng ShenNeuromolecular Biology Laboratory, The First Affiliated Hospital, and College of Clinical Medicine of Henan University of Science and Technology, Luoyang, 471003, China.
Yongjiang ZhangNeuromolecular Biology Laboratory, The First Affiliated Hospital, and College of Clinical Medicine of Henan University of Science and Technology, Luoyang, 471003, China.ORCID http://orcid.org/0000-0002-2728-0546
Menghan JiangDepartment of Neurology, The First Affiliated Hospital, and College of Clinical Medicine of Henan University of Science and Technology, Luoyang, 471003, China.
Anran LiuDepartment of Neurology, The First Affiliated Hospital, and College of Clinical Medicine of Henan University of Science and Technology, Luoyang, 471003, China.
Hongxia MaDepartment of Neurology, The First Affiliated Hospital, and College of Clinical Medicine of Henan University of Science and Technology, Luoyang, 471003, China.
Xiaoyi LaiNeuromolecular Biology Laboratory, The First Affiliated Hospital, and College of Clinical Medicine of Henan University of Science and Technology, Luoyang, 471003, China.
Jiannan WuNeuromolecular Biology Laboratory, The First Affiliated Hospital, and College of Clinical Medicine of Henan University of Science and Technology, Luoyang, 471003, China. wujiannan_haust@126.com.ORCID http://orcid.org/0000-0001-6018-4612
First Affiliated Hospital of Henan University of Science and Technology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The progression of Parkinson's disease (PD) is often accompanied by the loss of substantia nigra dopaminergic neurons, mitophagy damage, learning, and memory impairment. Idebenone is a therapeutic drug that targets the mitochondria of neurodegenerative diseases, but its role in Parkinson's disease and its pathological mechanism are still unclear. The purpose of this study was to investigate whether idebenone could improve behavioral disorders, especially motor, learning, and memory disorders, in mouse PD models and to explore its molecular mechanism. In the present study, C57BL-6 mice underwent intraperitoneal injection of MPTP (30 mg/kg) once a day for five consecutive days. Then, a 200 mg/kg dose was given as a single daily gavage of idebenone dissolved in water for 21 days after the successful establishment of the subacute MPTP model. Motor, learning, and memory were measured by a water maze and a rotarod test. Our results showed that idebenone could reduce MPTP-induced dopaminergic neuron damage and improve movement disorders, memory, and learning ability, which may be associated with upregulating mitochondrial autophagy-related outer membrane proteins VDAC1 and BNIP3 and activating the Parkin/PINK1 mitochondrial autophagy pathway. To confirm whether idebenone promotes the smooth progression of autophagy, we used eGFP-mCherry-LC3 mice to construct a subacute model of Parkinson's disease and found that idebenone can increase autophagy in dopaminergic neurons in Parkinson's disease. In summary, our results confirm that idebenone can regulate the expression of the mitochondrial outer membrane proteins VDAC1 and BNIP3, activate Parkin/PINK1 mitophagy, promote the degradation of damaged mitochondria, reduce dopaminergic neuron damage, and improve behavioral disorders in Parkinson's disease mice.

Identifiers

PMID35039479
PMCPMC8764058
OpenAlexW4206063295

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.