ArticleAntioxidants (Basel, Switzerland)2023
Dimethyl Itaconate Inhibits Melanogenesis in B16F10 Cells.
Article in Antioxidants (Basel, Switzerland), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed, 8 citations in OpenAlex.
- Itaconate and its derivatives in human health and diseases.Signal transduction and targeted therapy · 2026Review
- Cold atmospheric plasma (CAP) stimulates melanoblast-to-melanocyte differentiation via PRKCQ upregulation and NF-κB activation.iScience · 2026Article
- Regulation of melanin synthesis in goat hair follicles by melatonin through the Wnt/β-catenin pathway.Molecular genetics and genomics : MGG · 2025Article
- Inhibitory Effects of Fermented Sprouted Oat Extracts on Oxidative Stress and Melanin Overproduction.Antioxidants (Basel, Switzerland) · 2024Article
- Phenolic acids inJournal of ginseng research · 2023Article
- Anti-Melanogenic Effects ofPlants (Basel, Switzerland) · 2023Article
- Article
- The Effects of 2International journal of molecular sciences · 2023Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Itaconate is a metabolite produced to counteract and resolve pro-inflammatory responses when macrophages are challenged with intracellular or extracellular stimuli. In the present study, we have observed that dimethyl itaconate (DMI) inhibits melanogenesis in B16F10 cells. DMI inhibits microphthalmia-associated transcription factor (MITF) and downregulates the expression of MITF target genes, such as tyrosinase (TYR), tyrosinase-related protein 1 (TRP-1), and tyrosinase-related protein 2 (TRP-2). DMI also decreases the level of melanocortin 1 receptor (MC1R) and the production of α-melanocyte stimulating hormone (α-MSH), resulting in the inhibition of extracellular signal-regulated kinase 1/2 (ERK1/2) and MITF activities. The structure-activity relationship (SAR) study illustrates that the α,β-unsaturated carbonyl moiety in DMI, a moiety required to target KELCH-like ECH-associated protein 1 (KEAP1) to activate NF-E2-related factor 2 (NRF2), is necessary to inhibit melanogenesis and knocking down Nrf2 attenuates the inhibition of melanogenesis by DMI. Together, our study reveals that the MC1R-ERK1/2-MITF axis regulated by the KEAP1-NRF2 pathway is the molecular target responsible for the inhibition of melanogenesis by DMI.
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Registered trials
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 Socratic graph.