GCI Magazine

Segments Sponsored by

Email This Item!
Increase Text Size

Senescence: Reversing the Clock on Skin Aging

By: Shyam Gupta, PhD, and Linda Walker
Posted: April 4, 2012, from the April 2012 issue of GCI Magazine.

Aging in mammals remains an unsolved mystery,1 but one that science, beauty brands and consumers would love to solve. Anti-aging itself is a recurring topic in the history of scientific research—and has become one of the primary targets of many cosmetic products. In fact, consumers across age and gender categories are increasingly drawn to anti-aging products, demanding more from their brands. Understanding senescence, the change in the biology of an organism as it ages after its maturity, may be a key to unlocking the next step for anti-aging products; more accurately, treatments based on anti-senescence could offer a magic bullet, single solution for the myriad causes and signs of aging skin.

These changes range from those affecting cells and their function to those impacting the whole organism. Senescence is not universal, and senescence is not observed in single-celled organisms that reproduce through the process of cellular mitosis. Cellular senescence in humans causes the cells to stop replicating themselves through the process of mitosis, resulting in a buildup of senescent cells in the body. The body’s ability to clear these cells decreases with age, and that triggers cellular degradation over a period of time.

The importance of cell senescence to the aging process has long been suspected. The latest research demonstrates that these cells play a role in age-related cellular degradation, including skin aging. When cells become senescent, they produce inflammatory biological agents that initiate chronic tissue inflammation leading to age-related ailments such as dementia, diabetes and skin aging.2

Anti-senescence has been proposed as a novel therapeutic strategy for vascular aging.3 The vascular cells have a finite life span when cultured in vitro, and eventually enter an irreversible growth arrest state called “cellular senescence.” Recently, senescent vascular cells have been demonstrated in human atherosclerotic lesions, a condition that damages tissue. Moreover, these cells cause increased levels of pro-inflammatory molecules, which initiate cellular inflammation—known to be one of the principal causes of skin aging (further discussion of inflammation is available in “Inflammation and Aging” [GCI March 2011], available at www.GCImagazine.com). The cascading effect of senescence on skin aging is thus clear.

Lessons From the Survivors of Hard Life