Evidence map›Paper›PMID 41520027›Full record

ArticleScientific reports2026

Disruption of intracellular iron homeostasis through mitochondrial dysfunction associated with suppression of ATP 13A2 expression.

Takanori Murakami, Kazuki Ohuchi, Masanori Kiuchi, Hisaka Kurita, Kanta Kawai, Ryo Kakiuchi, Tasuku Hirayama, Hideko Nagasawa, Zhiliang Wu, Yoichi Maekawa and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. 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

12 authors.

Takanori MurakamiLaboratory of Medical Therapeutics and Molecular Therapeutics, Gifu Pharmaceutical University, 1-25-4 Daigaku-Nishi, Gifu, Gifu, 501-1196, Japan.
Kazuki OhuchiLaboratory of Medical Therapeutics and Molecular Therapeutics, Gifu Pharmaceutical University, 1-25-4 Daigaku-Nishi, Gifu, Gifu, 501-1196, Japan.
Masanori KiuchiLaboratory of Medical Therapeutics and Molecular Therapeutics, Gifu Pharmaceutical University, 1-25-4 Daigaku-Nishi, Gifu, Gifu, 501-1196, Japan.
Hisaka KuritaLaboratory of Medical Therapeutics and Molecular Therapeutics, Gifu Pharmaceutical University, 1-25-4 Daigaku-Nishi, Gifu, Gifu, 501-1196, Japan.
Kanta KawaiLaboratory of Pharmaceutical and Medicinal Chemistry, Gifu Pharmaceutical University, 1-25-4 Daigaku-Nishi, Gifu, Gifu, 501-1196, Japan.
Ryo KakiuchiLaboratory of Pharmaceutical and Medicinal Chemistry, Gifu Pharmaceutical University, 1-25-4 Daigaku-Nishi, Gifu, Gifu, 501-1196, Japan.
Tasuku HirayamaLaboratory of Pharmaceutical and Medicinal Chemistry, Gifu Pharmaceutical University, 1-25-4 Daigaku-Nishi, Gifu, Gifu, 501-1196, Japan.
Hideko NagasawaLaboratory of Pharmaceutical and Medicinal Chemistry, Gifu Pharmaceutical University, 1-25-4 Daigaku-Nishi, Gifu, Gifu, 501-1196, Japan.
Zhiliang WuDepartment of Parasitology and Infectious Diseases, Gifu University Graduate School of Medicine, Gifu, 501-1194, Japan.
Yoichi MaekawaDepartment of Parasitology and Infectious Diseases, Gifu University Graduate School of Medicine, Gifu, 501-1194, Japan.
Isao HozumiLaboratory of Medical Therapeutics and Molecular Therapeutics, Gifu Pharmaceutical University, 1-25-4 Daigaku-Nishi, Gifu, Gifu, 501-1196, Japan.
Masatoshi IndenLaboratory of Medical Therapeutics and Molecular Therapeutics, Gifu Pharmaceutical University, 1-25-4 Daigaku-Nishi, Gifu, Gifu, 501-1196, Japan. inden@gifu-pu.ac.jp.

Funding

a Grant-in-Aid for Scientific Research on Innovative Areas JSPS KAKENHI JP19H05767A02Japan Society for the Promotion of Science 22K06744JST SPRING JPMJSP2142Smoking Research Foundation 2021G021
6 · The paper itself

Abstract

Elevated iron in the SNpc may play a key role in Parkinson's disease (PD) neurodegeneration, yet the underlying mechanism accounting for this iron accumulation is unclear. Although iron is an essential element, excessive amounts produce toxicity. Here, we focused on the role of iron and ATP13A2, the causative gene of PARK9 neurodegeneration with brain iron accumulation, using a cellular model. ATP13A2 deficiency resulted in impaired lysosomal function and iron accumulation in cell organelles. Further, we found dysfunction of mitophagy, which is involved in managing mitochondrial quality, as well as mitochondrial damage. Furthermore, we confirmed a decreased heme synthesis capacity, which is important to maintain intracellular iron homeostasis. Overall, our study indicates that lysosome-derived mitochondrial impairment can disrupt intracellular iron homeostasis in a cell model of PD pathology. This could help better understand the mechanisms underlying PD.

Indexed as

HomeostasisIronMitochondriaProton-Translocating ATPasesAnimalsHemeHumansIron Regulatory Protein 2LysosomesMitophagyParkinson DiseaseATP13A2 protein, humanHemeIronIron Regulatory Protein 2Proton-Translocating ATPasesATP13A2HemeIntracellular iron homeostasisIRP2LysosomeMitochondriaMitophagyPARK9Parkinson’s diseaseTransferrin receptor

Identifiers

PMID41520027
PMCPMC12876906

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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 Socratic graph.