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

Scientific reports · 2025 · Benefit · Low evidence

← Research stream

BenefitLow evidencePaper 5893

Study snapshot

PublicationScientific reports · 2025

Study typein_vitro

Reported directionBenefit

Evidence ratingLow

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.

Machine Enhanced Logic

AI evidence extraction

Structured fields below were generated from the paper’s abstract and metadata to make the evidence easier to inspect. Automated extraction may be incomplete or incorrect; verify important details against the original paper.

Study typein_vitro

Effect directionbenefit

PopulationNot supplied

Sample sizeNot supplied

ExposureELF

Evidence strengthLowConfidence: 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.

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": 0.74,
  "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": 0.9,
      "reason": "Study examines mitochondrial transcription, OXPHOS activity, dynamics (DRP1/MFN1/MFN2), and ATP production under ELF-EMF exposure in vitro."
    }
  ]
}

AI can be wrong. Always verify against the paper.

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

Identifiers and source

DOI: 10.1038/s41598-025-10536-7
PubMed: 40629055

Read the original paper →

Related papers

← Back to the Research Library