ArticleInternational journal of molecular sciences2021
Marliolide Derivative Induces Melanosome Degradation via Nrf2/p62-Mediated Autophagy.
Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 17 citations in OpenAlex.
- Ganoderic Acid A Reverses Ultraviolet B Induced Hyperpigmentation via Multi-Targeted Regulation of Mitochondrial Homeostasis and Inflammation.Molecules (Basel, Switzerland) · 2026Article
- Emerging perspectives on the selective autophagy of melanosomes: melanophagy.Experimental & molecular medicine · 2025Review
- Melanosome Transport and Processing in Skin Pigmentation: Mechanisms and Targets for Pigmentation Modulation.International journal of molecular sciences · 2025Review
- Research progress on pathogenesis of skin pigmentation in chronic liver disease.Biomolecules & biomedicine · 2025Review
- The Pathogenesis of Oxidative Stress-Induced Chloasma and Its Therapeutic Implications.Clinical, cosmetic and investigational dermatology · 2025Review
- Ceramide Ehux-C22 Targets the miR-199a-3p/mTOR Signaling Pathway to Regulate Melanosomal Autophagy in Mouse B16 Cells.International journal of molecular sciences · 2024Article
- Melanin's Journey from Melanocytes to Keratinocytes: Uncovering the Molecular Mechanisms of Melanin Transfer and Processing.International journal of molecular sciences · 2023Review
- Alpha-Synuclein and Its Role in Melanocytes.Cells · 2022Article
- Review
- Dimethyl Itaconate Reduces α-MSH-Induced Pigmentation via Modulation of AKT and p38 MAPK Signaling Pathways in B16F10 Mouse Melanoma Cells.Molecules (Basel, Switzerland) · 2022Article
- Salidroside Ameliorates Ultraviolet-Induced Keratinocyte Injury by Inducing SIRT1-Dependent Autophagy.Clinical, cosmetic and investigational dermatology · 2022Article
- Implications of Oxidative Stress in the Pathogenesis and Treatment of Hyperpigmentation Disorders.Oxidative medicine and cellular longevity · 2022Review
- Evaluating Whether Radiofrequency Irradiation Attenuated UV-B-Induced Skin Pigmentation by Increasing Melanosomal Autophagy and Decreasing Melanin Synthesis.International journal of molecular sciences · 2021Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Nuclear factor erythroid 2-related factor 2 (Nrf2), which is linked to autophagy regulation and melanogenesis regulation, is activated by marliolide. In this study, we investigated the effect of a marliolide derivative on melanosome degradation through the autophagy pathway. The effect of the marliolide derivative on melanosome degradation was investigated in α-melanocyte stimulating hormone (α-MSH)-treated melanocytes, melanosome-incorporated keratinocyte, and ultraviolet (UV)B-exposed HRM-2 mice (melanin-possessing hairless mice). The marliolide derivative, 5-methyl-3-tetradecylidene-dihydro-furan-2-one (DMF02), decreased melanin pigmentation by melanosome degradation in α-MSH-treated melanocytes and melanosome-incorporated keratinocytes, evidenced by premelanosome protein (PMEL) expression, but did not affect melanogenesis-associated proteins. The UVB-induced hyperpigmentation in HRM-2 mice was also reduced by a topical application of DMF02. DMF02 activated Nrf2 and induced autophagy in vivo, evidenced by decreased PMEL in microtubule-associated proteins 1A/1B light chain 3B (LC3)-II-expressed areas. DMF02 also induced melanosome degradation via autophagy in vitro, and DMF02-induced melanosome degradation was recovered by chloroquine (CQ), which is a lysosomal inhibitor. In addition, Nrf2 silencing by siRNA attenuated the DMF02-induced melanosome degradation via the suppression of p62. DMF02 induced melanosome degradation in melanocytes and keratinocytes by regulating autophagy via Nrf2-p62 activation. Therefore, Nrf2 activator could be a promising therapeutic agent for reducing hyperpigmentation.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.