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Tranexamic Acid Inhibits 17β-Estradiol-Induced Melanogenesis Through PKA-CREB-MITF Pathway
Yu Jeong Bae1, Eun Jung Lee1, Ji Young Kim1
1Department of Dermatology and Cutaneous Biology Research Institute, Yonsei University College of Medicine, Seoul, Korea.
Experimental Dermatology
|December 15, 2025
Summary
Tranexamic acid (TXA) effectively treats hyperpigmentation by inhibiting estrogen-induced melanogenesis. It works by downregulating the cAMP-PKA pathway, suggesting a role in modulating the cAMP-PKA-CREB-MITF axis for depigmentation.
Area of Science:
- Dermatology
- Molecular Biology
- Biochemistry
Background:
- Melasma, a common hyperpigmentation disorder, is often linked to estrogen.
- Estrogen can induce skin pigmentation via estrogen receptors.
- The precise mechanism of tranexamic acid's (TXA) effect on estrogen-induced pigmentation is not fully understood.
Purpose of the Study:
- To investigate the effect of TXA on 17β-estradiol (E2)-induced melanogenesis.
- To elucidate the molecular pathways involved in TXA's anti-pigmentation effects.
Main Methods:
- Primary human epidermal melanocytes were used.
- Cell viability was assessed after treatment with E2 or TXA.
- Western blot analysis measured protein levels of p-CREB, MITF, and tyrosinase.
Main Results:
- 17β-estradiol increased melanin production by upregulating p-CREB, MITF, and tyrosinase.
- TXA inhibited E2-induced melanogenesis.
- TXA downregulated the cAMP-PKA pathway and modulated the cAMP-PKA-CREB-MITF axis.
Conclusions:
- TXA inhibits estrogen-induced melanogenesis.
- TXA's depigmenting effect is likely mediated by modulating the cAMP-PKA-CREB-MITF signaling pathway.
- TXA offers a potential therapeutic strategy for estrogen-mediated hyperpigmentation.
