Vitiligo pp 329-332 | Cite as

Other Defects/Mechanisms

  • Maria Lucia Dell’Anna
  • Mauro PicardoEmail author


Vitiligo pathogenesis still represents a puzzle whose pieces are not all at the same level of knowledge and interest among the scientist people. The most popular aspects currently considered include genetic, inflammatory, autoimmune, oxidative, and metabolic alterations, even if the individual contribution of each of these alterations is still unclear. The role of local environment, detachment process and emerging pathways needs renewed attention. These pieces of vitiligo puzzle represent a possible link between the most studied mechanisms and all three together are supporting each other.


  1. 1.
    Picardo M, Dell’Anna ML, Ezzedine K, Hamzavi I, Harris JE, Parsad D, et al. Vitiligo. Nat Rev Dis Primers. 2015;1:15011.PubMedCrossRefGoogle Scholar
  2. 2.
    Bellei B, Pitisci A, Ottaviani M, Ludovici M, Cota C, Luzi F, et al. Vitiligo: a possible model of degenerative diseases. PLoS One. 2013;8(3):e59782.PubMedPubMedCentralCrossRefGoogle Scholar
  3. 3.
    Bondanza S, Maurelli R, Paterna P, Migliore E, Giacomo FD, Primavera G, et al. Keratinocyte cultures from involved skin in vitiligo patients show an impaired in vitro behaviour. Pigment Cell Res. 2007;20(4):288–300.PubMedCrossRefGoogle Scholar
  4. 4.
    Kostyuk VA, Potapovich AI, Cesareo E, Brescia S, Guerra L, Valacchi G, et al. Dysfunction of glutathione S-transferase leads to excess 4-hydroxy-2-nonenal and H(2)O(2) and impaired cytokine pattern in cultured keratinocytes and blood of vitiligo patients. Antioxid Redox Signal. 2010;13(5):607–20.PubMedCrossRefGoogle Scholar
  5. 5.
    Kitamura R, Tsukamoto K, Harada K, Shimizu A, Shimada S, Kobayashi T, et al. Mechanisms underlying the dysfunction of melanocytes in vitiligo epidermis: role of SCF/KIT protein interactions and the downstream effector, MITF M. J Pathol. 2004;202(4):463–75.PubMedCrossRefGoogle Scholar
  6. 6.
    Kovacs D, Cardinali G, Aspite N, Cota C, Luzi F, Bellei B, et al. Role of fibroblast-derived growth factors in regulating hyperpigmentation of solar lentigo. Br J Dermatol. 2010;163(5):1020–7.PubMedCrossRefGoogle Scholar
  7. 7.
    Lee AY, Kim NH, Choi WI, Youm YH. Less keratinocyte-derived factors related to more keratinocyte apoptosis in depigmented than normally pigmented suction-blistered epidermis may cause passive melanocyte death in vitiligo. J Invest Dermatol. 2005;124(5):976–83.PubMedCrossRefGoogle Scholar
  8. 8.
    Le Poole IC, van den Wijngaard RM, Westerhof W, Das PK. Tenascin is overexpressed in vitiligo lesional skin and inhibits melanocyte adhesion. Br J Dermatol. 1997;137(2):171–8.PubMedCrossRefGoogle Scholar
  9. 9.
    Oh SH, Kim JY, Kim MR, Do JE, Shin JY, Hann SK. DKK1 is highly expressed in the dermis of vitiligo lesion: is there association between DKK1 and vitiligo? J Dermatol Sci. 2012;66(2):163–5.PubMedCrossRefGoogle Scholar
  10. 10.
    Purpura V, Persechino F, Belleudi F, Scrofani C, Raffa S, Persechino S, et al. Decreased expression of KGF/FGF7 and its receptor in pathological hypopigmentation. J Cell Mol Med. 2014;18(12):2553–7.PubMedPubMedCentralCrossRefGoogle Scholar
  11. 11.
    Briganti S, Flori E, Bellei B, Picardo M. Modulation of PPARγ provides new insights in a stress induced premature senescence model. PLoS One. 2014;9(8):e104045.PubMedPubMedCentralCrossRefGoogle Scholar
  12. 12.
    Kuang HB, Miao CL, Guo WX, Peng S, Cao YJ, Duan EK. Dickkopf-1 enhances migration of HEK293 cell by beta-catenin/E-cadherin degradation. Front Biosci (Landmark Ed). 2009;14:2212–20.CrossRefGoogle Scholar
  13. 13.
    Wagner RY, Luciani F, Cario-André M, Rubod A, Petit V, Benzekri L, et al. Altered E-cadherin levels and distribution in melanocytes precede clinical manifestations of vitiligo. J Invest Dermatol. 2015;135(7):1810–9.PubMedCrossRefGoogle Scholar
  14. 14.
    Ricard AS, Pain C, Daubos A, Ezzedine K, Lamrissi-Garcia I, Bibeyran A, Guyonnet-Dupérat V, Taieb A, Cario-André M. Study of CCN3 (NOV) and DDR1 in normal melanocytes and vitiligo skin. Exp Dermatol. 2012;21(6):411–6.PubMedCrossRefGoogle Scholar
  15. 15.
    Akiba S, Chiba M, Mukaida Y, Sato T. Involvement of reactive oxygen species and SP-1 in fibronectin production by oxidized LDL. Biochem Biophys Res Commun. 2003;310(2):491–7.PubMedCrossRefGoogle Scholar
  16. 16.
    Desmoulière A, Geinoz A, Gabbiani F, Gabbiani G. Transforming growth factor-beta 1 induces alpha-smooth muscle actin expression in granulation tissue myofibroblasts and in quiescent and growing cultured fibroblasts. J Cell Biol. 1993;122(1):103–11.PubMedCrossRefGoogle Scholar
  17. 17.
    Miyazaki M, Gohda E, Kaji K, Namba M. Increased hepatocyte growth factor production by aging human fibroblasts mainly due to autocrine stimulation by interleukin-1. Biochem Biophys Res Commun. 1998;246(1):255–60.PubMedCrossRefGoogle Scholar
  18. 18.
    Nishio K, Inoue A, Qiao S, Kondo H, Mimura A. Senescence and cytoskeleton: overproduction of vimentin induces senescent-like morphology in human fibroblasts. Histochem Cell Biol. 2001;116(4):321–7.PubMedCrossRefGoogle Scholar
  19. 19.
    Powell DW, Mifflin RC, Valentich JD, Crowe SE, Saada JI, West AB. Myofibroblasts. I. Paracrine cells important in health and disease. Am J Phys. 1999;277(1 Pt 1):C1–9.Google Scholar
  20. 20.
    Waldera Lupa DM, Kalfalah F, Safferling K, Boukamp P, Poschmann G, Volpi E, et al. Characterization of skin aging-associated secreted proteins (SAASP) produced by dermal fibroblasts isolated from intrinsically aged human skin. J Invest Dermatol. 2015;135(8):1954–68.PubMedCrossRefGoogle Scholar
  21. 21.
    Yamaguchi Y, Itami S, Watabe H, Yasumoto K, Abdel-Malek ZA, Kubo T, et al. Mesenchymal-epithelial interactions in the skin: increased expression of dickkopf1 by palmoplantar fibroblasts inhibits melanocyte growth and differentiation. J Cell Biol. 2004;165(2):275–85.PubMedPubMedCentralCrossRefGoogle Scholar
  22. 22.
    Regazzetti C, Joly F, Marty C, Rivier M, Mehul B, Reiniche P, Mounier C, Rival Y, Piwnica D, Cavalié M, Chignon-Sicard B, Ballotti R, Voegel J, Passeron T. Transcriptional analysis of vitiligo skin reveals the alteration of WNT pathway: a promising target for repigmenting vitiligo patients. J Invest Dermatol. 2015;135(12):3105–14.PubMedCrossRefGoogle Scholar

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© Springer Nature Switzerland AG 2019

Authors and Affiliations

  1. 1.Cutaneous PhysiopathologySan Gallicano Dermatological Institute, IFORomeItaly

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