ReviewFrontiers in pain research (Lausanne, Switzerland)2026
The effects of pulsed radiofrequency stimulation on mitochondrial function in neurons: a mini review.
Review in Frontiers in pain research (Lausanne, Switzerland), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
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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.
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.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pulsed radiofrequency (PRF) stimulation is a widely used clinical intervention for neuropathic pain. Unlike continuous radiofrequency (CRF) ablation, PRF is non-destructive, yet its precise mechanism of action remains under debate. Emerging evidence suggests a fundamental role of mitochondrial modulation in driving both analgesia and nerve regeneration. To synthesize the literature investigating PRF effects on neuronal mitochondrial function, a scoping review was conducted across five databases (MEDLINE, Embase, CENTRAL, Web of Science, PubMed) from inception to February 2, 2026. From 141 initial records, 10 experimental studies met the inclusion criteria for narrative synthesis. Four studies comparing PRF with CRF confirmed that while CRF induces severe mitochondrial pathology (swelling, cristolysis, and necrosis), PRF preserves mitochondrial ultrastructure. The remaining six studies identified specific bioenergetic mechanisms. PRF was found to actively decrease mitochondrial membrane potential (
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