Evidence map›Paper›PMID 40629055›Full record

ArticleScientific reports2025

Extremely low-frequency electromagnetic field (ELF-EMF) enhances mitochondrial energy production in NARP cybrids.

Mikako Ito, Zhizhou Huang, Kosaku Nomura, Masaki Teranishi, Fei Zhao, Hiroyuki Mino, Makoto Yoneda, Masashi Tanaka, Kinji Ohno

Abstract read
In one paragraph

Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Trial
  2. 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.

Mikako Ito *Division of Neurogenetics, Center for Neurological Diseases and Cancer, Nagoya University Graduate School of Medicine, Nagoya, Japan. ito@med.nagoya-u.ac.jp.
Zhizhou Huang *Division of Neurogenetics, Center for Neurological Diseases and Cancer, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Kosaku NomuraDivision of Neurogenetics, Center for Neurological Diseases and Cancer, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Masaki TeranishiDivision of Neurogenetics, Center for Neurological Diseases and Cancer, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Fei ZhaoDivision of Neurogenetics, Center for Neurological Diseases and Cancer, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Hiroyuki MinoDivision of Material Science (Physics), Graduate School of Science, Nagoya University, Nagoya, Japan.
Makoto YonedaGraduate School of Health and Human Life Sciences, Fukui Prefectural University, Fukui, Japan.
Masashi TanakaDepartment of Neurology, Juntendo University Graduate School of Medicine, Tokyo, Japan.
Kinji OhnoDivision of Neurogenetics, Center for Neurological Diseases and Cancer, Nagoya University Graduate School of Medicine, Nagoya, Japan. ohnok@med.nagoya-u.ac.jp.

Funding

Japan Agency for Medical Research and Development JP23ek0109678Japan Society for the Promotion of Science JP23H02794Japan Society for the Promotion of Science JP23K06412Ministry of Health, Labour and Welfare 23FC1014National Center of Neurology and Psychiatry 5-6
6 · The paper itself

Abstract

A mutation (m.8993T > G) in MT-ATP6 in mitochondrial DNA (mtDNA) causes the neuropathy, ataxia, retinitis pigmentosa (NARP) syndrome by impairing mitochondrial energy production. Extremely low-frequency electromagnetic field (ELF-EMF) suppresses mitochondrial oxidative phosphorylation (OXPHOS) Complex II and induces mitohormetic activation of mitochondrial OXPHOS activities. We examined the effects of ELF-EMF on normal cybrids carrying 100% wild-type mtDNA (2SA cybrids) and NARP cybrids carrying 40% wild-type and 60% mutant mtDNA (NARP3-2 cybrids). We found that ELF-EMF had no effect on the copy number of mtDNA either in 2SA or NARP3-2 cybrids, or the ratio of wild-type-to-mutant mtDNA in NARP3-2 cybrids. Instead, ELF-EMF increased the transcription of mtDNA and the transcription ratio of wild-type-to-mutant mtDNA in NARP3-2 cybrids. In addition, ELF-EMF increased the expression of mitochondrial OXPHOS proteins and the mitochondrial OXPHOS Complex V activity in NARP3-2 cybrids. ELF-EMF upregulated fission-promoting phosphorylation of DRP1, as well as the expression of fusion-promoting MFN1 and MFN2, in NARP3-2 cybrids. ELF-EMF also increased ATP production estimated by oxygen consumption rates (OCR) and by a biochemical assay in NARP3-2 cybrids. Hormetic activation of mitochondria by ELF-EMF is likely to be effective to ameliorate defective mitochondrial energy production in NARP and other mitochondrial diseases.

Indexed as

Electromagnetic FieldsEnergy MetabolismMitochondriaRetinitis PigmentosaDNA, MitochondrialHumansMitochondrial MyopathiesMitochondrial ProteinsMutationOxidative PhosphorylationDNA, MitochondrialMitochondrial ProteinsAnd mitohormesisExtremely low-frequency electromagnetic field (ELF-EMF)Mitochondrial biogenesisMitochondrial DNAMitophagyNeuropathy, ataxia, retinitis pigmentosa (NARP) syndrome

Identifiers

PMID40629055
PMCPMC12238397

What Socratic 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 Socratic graph.