Cell-communicating ingredients, theoretically, have the ability to tell a skin cell to look, act, and behave better, more like a normal healthy skin cell, or to stop other substances from telling the cell to behave badly or abnormally. They do this by either direct communication with the skin cell or by blocking damaging cellular pathways or other cell-communicating substances.
For all parts of our bodies to work properly, including skin cells, each cell must know how to perform the correct action at the correct time—and, hopefully, to ignore information (in the form of messenger substances) that tells cells to do the wrong thing. This takes place through constant communication, with many substances telling cells how and when to function properly, and the cells then relaying that information to each other. When cells have a miscommunication, or when substances relaying bad information get through to the cell, it can cause all sorts of problems. Every cell has a vast series of receptor sites for different substances; think of these receptor sites as the cell’s communication hookup. When the right ingredient for a specific site shows up, it has the ability to attach itself to the cell and transmit information. In the case of skin, this means telling the cell to start doing the things a healthy skin cell should be doing. If the cell accepts the message, the cell can then share the same healthy message with other nearby cells and so on and so on. [1, 2, 3, 4, 5, 6, 7, 8]
Theoretically, this area of investigation is incredibly exciting for skincare. For now, the skincare ingredients to look for in terms of cell-communicating ability include retinol, retinaldehyde, retinoic acid, epigallocatechin-3-gallate, eicosapentaenoic acid, niacinamide, lecithin, linolenic acid, linoleic acid, phospholipids, carnitine, carnosine, adenosine triphosphate, adenosine cyclic phosphate, most peptides, and Pyrus malus (apple) fruit extract.
- Lloyd S, Modlin R. Toll-like receptors in the skin.. Semin Immunopathol. 2007.;29(1):15-26.
- Kim M, Kim Y, Eun H, Cho K, Chung J. All-Trans Retinoic Acid Antagonizes UV-Induced VEGF Production and Angiogenesis via the Inhibition of ERK Activation in Human Skin Keratinocytes.. J Invest Dermatol. 2006;126(12):2697-2706.
- Li J, Zhang Y, Kirsner R. Angiogenesis in wound repair: angiogenic growth factors and the extracellular matrix.. Microsc Res Tech. 2003;60(1):107-14.
- He Z, Ong C, Halper J, Bateman A. Progranulin is a mediator of the wound response. Nat Med.. 2003;9(2):225-9.
- Quan T, He T, Kang S, Voorhees J, Fisher G. Connective tissue growth factor: expression in human skin in vivo and inhibition by ultraviolet irradiation.. J Invest Dermatol.. 2002;118(3):402-8.
- Denning M. Epidermal keratinocytes: regulation of multiple cell phenotypes by multiple protein kinase C isoforms. Int J Biochem Cell Biol.. 2004;36(7):1141-6.
- Boudjelal M, Voorhees J, Fisher G. Retinoid signaling is attenuated by proteasome-mediated degradation of retinoid receptors in human keratinocyte HaCaT cells.. Exp Cell Res.. 2002;274(1):130-7.
- de Gruijl F. Photocarcinogenesis: UVA vs. UVB Radiation. Skin Pharmacol Appl Skin Physiol.. 2002;15:316–320.