- Vitiligo is characterized by the functional loss of melanocytes which induces the well delineated depigmented characteristic lesions.
- Anomalies have been detected in:
- melanocytes (mitochondria…)
- keratinocytes (altered oxydation status in the mitochondria, vaculolization…)
- dermis (high level of tenascin expression which explains defective adhesion of the melanocytes)
- The authors have found similar defects in fibroblast cells in the dermis when compared to normal fibroblasts:
- altered membrane lipid (mainly cholesterol and cardiolipin) probably secondary to:
- reactive oxygen species (ROS) hyperproduction.
- deregulation of lipid-mediated intracellular signalling:
- ERK and JNK phosphorylation
- altered p38
Conclusion: normalization of fibroblast membrane structure could be crucial to improving vitiligo
Source of Information: Possible dermal involvement in vitiligo pathogenesis. M Dell’Anna, D Kovacs, M Ottaviani, E Bastonini and M Picardo Lab Cutaneous Physiopathology & CIRM, San Gallicano Dermatologic Institute, Rome, Italy. International Investigative Dermatology (IID) 2013 – Edinburgh, United Kingdom (UK).
Original article: here