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Melanin Pigmentation: Physiology and Pathology
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Melanin Pigmentation: Physiology and Pathology

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 20 March 2026 | Viewed by 531

Special Issue Editors

Prof. Dr. Shosuke Ito

E-Mail Website
Guest Editor
Department of Chemistry, Fujita Health University School of Health Sciences, Toyoake, Aichi, Japan
Interests: structure and properties of melanins; chemistry of melanogenesis; chemical analysis of melanins; effects of ultraviolet radiation and visible light on melanins; effects of heat on melanins; chemistry of tyrosinase-catalyzed oxidation of phenols
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Manickam Sugumaran

E-Mail Website
Guest Editor
Department of Biology, University of Massachusetts Boston, 100 Morrissey Blvd, Boston, MA 02125, USA
Interests: enzymology; post translational modifications; aromatic metabolism; phenolic biochemistry; reactions of quinonoid compounds; invertebrate immunity; insect cuticular sclerotization; phenoloxidase; quinone isomerases; oxidative browning; melanin biosynthesis; catecholic antibiotics
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Melanins are a group of biopolymeric phenolic pigments ubiquitously present in most organisms. In mammals and birds, two types of melanin are found, the brown-to-black insoluble eumelanin and the reddish-brown, sulfur-containing pheomelanin. They are produced within melanocytes through the tyrosinase-catalyzed oxidation of tyrosine. In addition, we are aware of extracutaneous melanins, such as substantia nigra neuromelanin. Studies have disclosed a variety of physiological roles for eumelanin, such as photoprotection, antioxidant defense, and drug/metal binding. On the contrary, pheomelanin is believed to be pro-oxidant and phototoxic, leading to melanoma development. Many factors are involved in the melanogenic pathway, and the dysregulation of these control mechanisms results in pigmentary disorders, from melasma to vitiligo.

Contributions to this Special Issue may cover any aspect of the chemistry of natural and synthetic melanins with potential practical applications; melanogenesis inhibition through the definition of its mechanism of action; approaches to the amelioration or control of any type of melanin-based pigmentary disorder, as well as photoprotection strategies; innovative methodologies for the analysis of pigmented tissues and for diagnostic purposes; molecular engineering methodologies for melanin production in microorganisms; and novel functions of melanins that are of potential interest for applications, drug targeting, and exploiting the specific affinities of melanins.

Experimental papers and up-to-date review articles are welcome.

Prof. Dr. Shosuke Ito
Prof. Dr. Manickam Sugumaran
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • eumelanin
  • pheomelanin
  • melanogenesis
  • photoprotection
  • pigmentary disorders
  • depigmenting agents
  • extracutaneous melanins

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Published Papers (2 papers)

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Research

13 pages, 4972 KB  
Article
Mechanistic Insights into Tyrosinase-Catalyzed Metabolism of Hydroquinone: Implications for the Etiology of Exogenous Ochronosis and Cytotoxicity to Melanocytes
by Shosuke Ito, Ludger Kolbe, Tamara Rogers, Tobias Mann, Gudrun Weets, Hitomi Tanaka, Tomoko Nishimaki-Mogami, Thierry Passeron, Makoto Ojika and Kazumasa Wakamatsu
Int. J. Mol. Sci. 2025, 26(21), 10734; https://doi.org/10.3390/ijms262110734 - 4 Nov 2025
Abstract
The metabolism of hydroquinone (HQ) by tyrosinase presents significant biochemical and dermatological challenges, particularly due to its association with adverse effects such as exogenous ochronosis (EO). Despite its widespread use in skin-lightening products, the detailed mechanistic pathways of HQ metabolism by tyrosinase remain [...] Read more.
The metabolism of hydroquinone (HQ) by tyrosinase presents significant biochemical and dermatological challenges, particularly due to its association with adverse effects such as exogenous ochronosis (EO). Despite its widespread use in skin-lightening products, the detailed mechanistic pathways of HQ metabolism by tyrosinase remain inadequately understood. This study aims to elucidate the mechanistic insights into the tyrosinase-catalyzed metabolism of HQ, leading to the production of HQ-eumelanin (HQ-EM) and HQ-pheomelanin (HQ-PM). We employed HPLC analysis to detect key intermediates and final metabolites. Results show that mushroom tyrosinase catalyzes the hydroxylation of HQ to 2-hydroxyhydroquinone (HHQ) via the 2-hydroxybenzoquinone (HBQ) pathway, giving rise to HQ-EM. However, in the presence of cysteine, a shift from HBQ to the benzoquinone (BQ) pathway occurs, giving rise to HQ-PM. Hydroiodic acid hydrolysis of HQ-PM and subsequent HPLC-electrochemical analysis identified 4-aminophenol (AP) as degradation product, thereby serving as a novel marker to monitor HQ oxidation in vitro. These results indicate that HQ functions both as a “pseudo” substrate for tyrosinase—undergoing redox exchange with dopaquinone to form BQ—and as a true substrate, yielding HBQ. This dual role contributes to the formation of HQ-EM and HQ-PM. It would be possible that EO is caused by a continuous oxidation of HQ mediated by tyrosinase activity in the skin. Full article
(This article belongs to the Special Issue Melanin Pigmentation: Physiology and Pathology)
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15 pages, 2409 KB  
Article
Over-Represented Senescent Keratinocytes in Hyperpigmented Spots Promote Melanocyte Activation via IGFBP3 and NGF
by Tomohiro Hakozaki, Holly Rovito, Bradley B. Jarrold, John Snowball, Jiazhen Wang, Wenzhu Zhao and Timothy Laughlin
Int. J. Mol. Sci. 2025, 26(21), 10724; https://doi.org/10.3390/ijms262110724 - 4 Nov 2025
Abstract
The occurrence and impact of cellular senescence on skin aging and hyperpigmentation is an ongoing area of exploration, encompassing both intrinsic and extrinsic stressors. Traditionally, research has focused on melanocyte and fibroblast senescence due to their slower turnover compared to keratinocytes. In this [...] Read more.
The occurrence and impact of cellular senescence on skin aging and hyperpigmentation is an ongoing area of exploration, encompassing both intrinsic and extrinsic stressors. Traditionally, research has focused on melanocyte and fibroblast senescence due to their slower turnover compared to keratinocytes. In this study, we identified the accumulation of p16, a senescence marker, in keratinocytes from biopsies of multiple spot types. We explored their impact using doxorubicin-induced senescent keratinocytes in vitro. Conditioned media from these senescent keratinocytes stimulated melanocyte dendricity, a hallmark of hyperpigmented spots. Transcriptomic analysis of senescent keratinocytes identified two key senescence-induced factors: Insulin-like Growth Factor-Binding Protein 3 (IGFBP3) and Nerve Growth Factor (NGF). IGFBP3 and NGF ligand treatment enhanced dendricity by 33% and 17%, and melanin synthesis by 23% and 14%, respectively, in human melanocyte cultures. These findings suggest that keratinocyte senescence contributes to spot formation by mediating melanocyte activation through IGFBP3 and NGF. Furthermore, we evaluated skincare ingredients such as sucrose dilaurate, glabridin, and niacinamide in neutral and low pH solutions, demonstrating their efficacy in reducing the secretion of these ligands, thereby offering potential cosmetic benefits. This study provides insights into the mechanisms of spot formation and highlights promising strategies for managing pigmentation disorders. Full article
(This article belongs to the Special Issue Melanin Pigmentation: Physiology and Pathology)
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