Evidence map›Paper›PMID 37282484›Full record

ArticleNeural regeneration research2023

Rapamycin reverses ferroptosis by increasing autophagy in MPTP/MPP

Tongyu Liu, Peihan Wang, Huan Yin, Xiangfei Wang, Jing Lv, Jiang Yuan, Jing Zhu, Yunfu Wang

Open access · goldAbstract read
In one paragraph

Article in Neural regeneration research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
9.7field-weighted citation impact, top 1% 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

27 citing papers in PubMed, 1 synthesis or guideline pooled it, 45 citations in OpenAlex.

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  17. Canonical and noncanonical autophagy: involvement in Parkinson's disease.Frontiers in cell and developmental biology · 2025
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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

8 authors at 2 institutions in 1 country.

Tongyu LiuDepartment of Neurology, Affiliated Taihe Hospital; Institute of Neuroscience, Hubei University of Medicine, Shiyan, Hubei Province, China.
Peihan WangDepartment of Neurology, Affiliated Taihe Hospital; Institute of Neuroscience, Hubei University of Medicine, Shiyan, Hubei Province, China.
Huan YinDepartment of Neurology, Affiliated Taihe Hospital; Institute of Neuroscience, Hubei University of Medicine, Shiyan, Hubei Province, China.
Xiangfei WangWudang Mountain Hospital Area of Taihe Hospital, Affiliated Hospital of Hubei University of Medicine, Shiyan, Hubei Province, China.
Jing LvDepartment of Neurology, Affiliated Taihe Hospital; Institute of Neuroscience, Hubei University of Medicine, Shiyan, Hubei Province, China.
Jiang YuanDepartment of Neurology, Affiliated Taihe Hospital, Hubei University of Medicine, Shiyan, Hubei Province, China.
Jing ZhuDepartment of Neurology, Affiliated Taihe Hospital; Institute of Neuroscience, Hubei University of Medicine; Wudang Mountain Hospital Area of Taihe Hospital, Affiliated Hospital of Hubei University of Medicine, Shiyan, Hubei Province, China.
Yunfu WangDepartment of Neurology, Affiliated Taihe Hospital; Institute of Neuroscience, Hubei University of Medicine, Shiyan, Hubei Province, China.
Hubei University of Medicine · CNTaihe Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Parkinson's disease is a neurodegenerative disorder, and ferroptosis plays a significant role in the pathological mechanism underlying Parkinson's disease. Rapamycin, an autophagy inducer, has been shown to have neuroprotective effects in Parkinson's disease. However, the link between rapamycin and ferroptosis in Parkinson's disease is not entirely clear. In this study, rapamycin was administered to a 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced Parkinson's disease mouse model and a 1-methyl-4-phenylpyridinium-induced Parkinson's disease PC12 cell model. The results showed that rapamycin improved the behavioral symptoms of Parkinson's disease model mice, reduced the loss of dopamine neurons in the substantia nigra pars compacta, and reduced the expression of ferroptosis-related indicators (glutathione peroxidase 4, recombinant solute carrier family 7, member 11, glutathione, malondialdehyde, and reactive oxygen species). In the Parkinson's disease cell model, rapamycin improved cell viability and reduced ferroptosis. The neuroprotective effect of rapamycin was attenuated by a ferroptosis inducer (methyl (1S,3R)-2-(2-chloroacetyl)-1-(4-methoxycarbonylphenyl)-1,3,4,9-tetrahyyridoindole-3-carboxylate) and an autophagy inhibitor (3-methyladenine). Inhibiting ferroptosis by activating autophagy may be an important mechanism by which rapamycin exerts its neuroprotective effects. Therefore, the regulation of ferroptosis and autophagy may provide a therapeutic target for drug treatments in Parkinson's disease.

Indexed as

autophagybehaviorferroptosisMPTPParkinson’s diseasePC12 cellrapamycintyrosine hydroxylase

Identifiers

PMID37282484
PMCPMC10360095
OpenAlexW4323967871

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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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.