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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