According to LVMH inventors, in the epidermis, NOTCH proteins ensure that cell proliferation and differentiation are coordinated to promote homeostasis; but this signaling can be lost with aging. In response, the company has identified a peppermint extract that can reinvigorate this signaling.
NOTCH proteins 1 and 2 belong to a family of transmembrane receptors that are activated by direct binding between the receptor and its ligands, borne by neighboring cells. However, as LVMH explains in a recent patent, dysfunctions in NOTCH signaling lead to major anomalies for the epidermis and its appendages, causing functional losses such as a defective cutaneous barrier or insufficient sebaceous production. Additional conditions can include atopy, vitiligo and even some cancers.
NOTCH Effects in Skin
The inventors note several studies that have converged to indicate cell signaling controlled by NOTCH proteins as essential for good skin repair and reportedly involved in the regulation of several phases of the wound healing process; especially in regulating angiogenesis during the production of the extracellular matrix, and in inflammation.
Identifying this biological target, LVMH researchers note that due to its stimulating action on NOTCH production in keratinocyte progenitor cells, peppermint extract is a particularly beneficial agent for maintaining or reinforcing the renewal of cells in the epidermis.
Cosmetic use of a peppermint extract
U.S. Pat 10413502
Publication date: Sep. 17, 2019
Assignee: LVMH Recherche
This invention relates to the use, in a cosmetic composition, of a peppermint extract as an agent intended to increase the renewal of cells in the epidermis associated with a deficiency in the expression of NOTCH proteins in keratinocyte progenitor cells; in particular, for mature skin and/or skin exhibiting signs of dryness and of loss of firmness. The invention also relates to a care method for maintaining or regulating the renewal of the cells of the epidermis associated with said deficiency.
Patent accessed on Dec. 20, 2019.