Vitiligo: A Diverse Perspective
Growing data support the involvement of all cutaneous cell populations in vitiligo in both lesional and non lesional skin. Our group previously demonstrated mitochondria-linked metabolic defects in melanocytes, generating high intracellular ROS levels, low ATP production and stress-mediated premature senescence phenotype. We detected similar intrinsic alterations also in fibroblasts, associated to the induction of autophagy in both cell types, as an adaptive/compensatory response to counteract the intrinsic vulnerability. Considering the mitochondrial metabolic impairment as the biochemical basis of the disease, we also extended our analysis on the structural and functional features of keratinocytes and skin barrier of normal-appearing skin. We highlighted alterations in the differentiation program with an undermined process of stratification and barrier assembly. We further showed an unbalanced in lipid composition of the stratum corneum, suggestive of impairment to develop a full-competent skin barrier. This barrier defect can constitute the prime defect causing the onset of a local inflammatory milieu able to activate innate and adapted immune responses targeting melanocytes and a possible cause of the occurence of the koebner phenomenon. The skin barrier can be pointed as a novel crucial player in the broad and complex field of the disease pathogenesis and may be efficiently targeted to provide protection even in skin areas where the lesions are not already clinically manifested.
D. Kovacs, E. Bastonini, M. Ottaviani, S. Briganti, L. Sciuto, M. Truglio, C. Cota, A. D’Arino, A. Pacifico, P. Iacovelli