Oxidative stress management in the hair follicle: Could targeting NRF2 counter age‐related hair disorders and beyond?
Widespread expression of the transcription factor, nuclear factor (erythroid‐derived 2)‐like 2 (NRF2), which maintains redox homeostasis, has recently been identified in the hair follicle (HF). Small molecule activators of NRF2 may therefore be useful in the management of HF pathologies associated w...
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Published in | BioEssays Vol. 39; no. 8 |
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Main Authors | , , , , , |
Format | Journal Article |
Language | English |
Published |
United States
Wiley Subscription Services, Inc
01.08.2017
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Subjects | |
Online Access | Get full text |
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Summary: | Widespread expression of the transcription factor, nuclear factor (erythroid‐derived 2)‐like 2 (NRF2), which maintains redox homeostasis, has recently been identified in the hair follicle (HF). Small molecule activators of NRF2 may therefore be useful in the management of HF pathologies associated with redox imbalance, ranging from HF greying and HF ageing via androgenetic alopecia and alopecia areata to chemotherapy‐induced hair loss. Indeed, NRF2 activation has been shown to prevent peroxide‐induced hair growth inhibition. Multiple parameters can increase the levels of reactive oxygen species in the HF, for example melanogenesis, depilation‐induced trauma, neurogenic and autoimmune inflammation, toxic drugs, environmental stressors such as UV irradiation, genetic defects and aging‐associated mitochondrial dysfunction. In this review, the potential mechanisms whereby NRF2 activation could prove beneficial in treatment of redox‐associated HF disorders are therefore discussed.
Accumulation of reactive oxygen species (ROS) is associated with certain hair disorders and exposure to exogenous stressors, being implicated in apoptosis, hair loss, hair miniaturization and melanocytes damage leading to hair greying. NRF2 activators such as sulforaphane (SFN) may protect against the progression of hair disorders associated with elevated ROS. |
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ISSN: | 0265-9247 1521-1878 |
DOI: | 10.1002/bies.201700029 |