Abstract Skin is subject to frequent friction injury. Friction affects different structures of the skin, including keratinocytes, melanocytes, fibroblasts, and follicular units. Friction can also stimulate cytokine production. Friction is sensed by the mechanoreceptors, resulting in signal transduction to the nucleus, activating transcription factors and mechanoresponsive genes. Numerous friction-aggravated diseases have been identified, including inflammatory, depositional, follicular, genetic, infectious, and vesiculobullous disorders. Friction, as a potential modifiable aggravator, should be considered when skin diseases are located at friction-prone areas.
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