ReviewJournal of tissue engineering
Bioelectric modulation of scar fate in wound repair: Mechanisms, dosimetry, and scar-oriented electroceutical design.
Review in Journal of tissue engineering. 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
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.
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
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Exogenous electrical stimulation accelerates cutaneous wound closure, but its effect on pathological scarring remains poorly defined. This review reframes the field around scar fate rather than closure speed and applies a three-tier endpoint framework that distinguishes wound closure, tissue-quality surrogates, and validated scar outcomes. We examine endogenous bioelectric signaling and evaluate how electrical stimulation influences electrotaxis, calcium-dependent myofibroblast activation, TGF beta signaling, extracellular matrix remodeling, and immune regulation. Current evidence shows that some platforms reduce collagen I, alpha smooth muscle actin, and myofibroblast activity, whereas other stimulation conditions enhance profibrotic signaling. These divergent effects are strongly dependent on dose, waveform, exposure time, cell source, and biological context. However, validated scar scales, mature scar outcomes, and rigorous fibroproliferative models remain rarely used in current experimental studies. We therefore propose a dosimetry and reporting framework to guide scar-oriented electroceutical design and clinical translation.
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Registered trials
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.