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Piperonylic Acid Promotes Hair Growth by Activation of EGFR and Wnt/β-Catenin Pathway. | LitMetric

Piperonylic Acid Promotes Hair Growth by Activation of EGFR and Wnt/β-Catenin Pathway.

Int J Mol Sci

Generative Genomics Research Center, Global Green Research & Development Center, Handong Global University, Pohang 37554, Republic of Korea.

Published: October 2024

AI Article Synopsis

  • * Piperonylic acid activates both EGFR and Wnt/β-catenin pathways in DPCs, enhancing cell growth and increasing markers associated with hair follicle formation.
  • * Clinical trials revealed that a formulation with piperonylic acid resulted in a significant increase in hair density compared to a placebo, highlighting its potential as a hair loss treatment.

Article Abstract

Dermal papilla cells (DPCs) are located at the bottom of the hair follicle and play a critical role in hair growth, shape, and cycle. Epidermal growth factor receptor (EGFR) and Wnt/β-catenin signaling pathways are essential in promoting keratinocyte activation as well as hair follicle formation in DPCs. Piperonylic acid is a small molecule that induces EGFR activation in keratinocytes. However, the effects of piperonylic acid on DPCs in regard to the stimulation of hair growth have not been studied. In the present study, piperonylic acid was shown to activate the Wnt/β-catenin signaling pathway in addition to the EGFR signaling pathway in DPCs. Piperonylic acid suppressed DKK1 expression, which presumably promoted the accumulation of β-catenin in the nucleus. In addition, piperonylic acid promoted cyclin D upregulation and cell growth and increased the expression of alkaline phosphatase (ALP), a DPC marker. In a clinical study, the group that applied a formulation containing piperonylic acid had a significantly higher number of hairs per unit area than the placebo group. These results identify piperonylic acid as a promising new candidate for hair loss treatment.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11476903PMC
http://dx.doi.org/10.3390/ijms251910774DOI Listing

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