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

PAPER pubmed Scientific reports 2025 In vitro study Effect: benefit Evidence: Low

Read original paper → DOI: 10.1038/s41598-025-10536-7 PMID: 40629055 Evidence Lab

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.

AI evidence extraction

At a glance

Study type

In vitro study

Effect direction

benefit

Population

—

Sample size

—

Exposure

ELF

Evidence strength

Low

Confidence: 74% · Peer-reviewed: yes

Main findings

In cybrid cell models, ELF-EMF had no effect on mtDNA copy number in either wild-type (2SA) or NARP (NARP3-2) cybrids, and did not change the wild-type-to-mutant mtDNA ratio in NARP3-2 cybrids. ELF-EMF increased mtDNA transcription and the wild-type-to-mutant mtDNA transcription ratio in NARP3-2 cybrids, increased mitochondrial OXPHOS protein expression and Complex V activity, altered fission/fusion-related markers (DRP1 phosphorylation, MFN1/MFN2 expression), and increased ATP production (including via OCR estimates) in NARP3-2 cybrids.

Outcomes measured

mtDNA copy number
wild-type-to-mutant mtDNA ratio
mtDNA transcription
wild-type-to-mutant mtDNA transcription ratio
mitochondrial OXPHOS protein expression
OXPHOS Complex V activity
DRP1 phosphorylation (fission-related)
MFN1 and MFN2 expression (fusion-related)
ATP production
oxygen consumption rate (OCR)

Limitations

Exposure parameters (e.g., frequency, field strength, duration) are not provided in the abstract.
In vitro cybrid model; findings may not generalize to humans or clinical outcomes.
Sample size and replication details are not stated in the abstract.

Suggested hubs

mechanisms-mitochondria (0.9)
Study examines mitochondrial transcription, OXPHOS activity, dynamics (DRP1/MFN1/MFN2), and ATP production under ELF-EMF exposure in vitro.

View raw extracted JSON

{
    "study_type": "in_vitro",
    "exposure": {
        "band": "ELF",
        "source": null,
        "frequency_mhz": null,
        "sar_wkg": null,
        "duration": null
    },
    "population": null,
    "sample_size": null,
    "outcomes": [
        "mtDNA copy number",
        "wild-type-to-mutant mtDNA ratio",
        "mtDNA transcription",
        "wild-type-to-mutant mtDNA transcription ratio",
        "mitochondrial OXPHOS protein expression",
        "OXPHOS Complex V activity",
        "DRP1 phosphorylation (fission-related)",
        "MFN1 and MFN2 expression (fusion-related)",
        "ATP production",
        "oxygen consumption rate (OCR)"
    ],
    "main_findings": "In cybrid cell models, ELF-EMF had no effect on mtDNA copy number in either wild-type (2SA) or NARP (NARP3-2) cybrids, and did not change the wild-type-to-mutant mtDNA ratio in NARP3-2 cybrids. ELF-EMF increased mtDNA transcription and the wild-type-to-mutant mtDNA transcription ratio in NARP3-2 cybrids, increased mitochondrial OXPHOS protein expression and Complex V activity, altered fission/fusion-related markers (DRP1 phosphorylation, MFN1/MFN2 expression), and increased ATP production (including via OCR estimates) in NARP3-2 cybrids.",
    "effect_direction": "benefit",
    "limitations": [
        "Exposure parameters (e.g., frequency, field strength, duration) are not provided in the abstract.",
        "In vitro cybrid model; findings may not generalize to humans or clinical outcomes.",
        "Sample size and replication details are not stated in the abstract."
    ],
    "evidence_strength": "low",
    "confidence": 0.7399999999999999911182158029987476766109466552734375,
    "peer_reviewed_likely": "yes",
    "keywords": [
        "ELF-EMF",
        "extremely low-frequency electromagnetic field",
        "mitochondria",
        "NARP syndrome",
        "MT-ATP6 m.8993T>G",
        "cybrids",
        "oxidative phosphorylation",
        "Complex V",
        "ATP production",
        "oxygen consumption rate",
        "DRP1",
        "MFN1",
        "MFN2",
        "mitohormesis"
    ],
    "suggested_hubs": [
        {
            "slug": "mechanisms-mitochondria",
            "weight": 0.90000000000000002220446049250313080847263336181640625,
            "reason": "Study examines mitochondrial transcription, OXPHOS activity, dynamics (DRP1/MFN1/MFN2), and ATP production under ELF-EMF exposure in vitro."
        }
    ]
}

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AI-extracted fields are generated from the abstract/metadata and may be incomplete or incorrect. This content is for informational purposes only and is not medical advice.

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