Skin is a perfect model organ for the study of aging: it’s large; it ages both chronologically and inducibly (via exposure to sun and toxins); and it’s on the outside of the body, so that therapeutics designed for the skin don’t have to be orally bioavailable or well-tolerated on the inside of the body.

As an added bonus, humans have already demonstrated their willingness to fork over huge amounts of cash to slow the aging process in this most visible of organs. There’s gold in them there laugh lines.

Hence I’ve started paying closer attention to the skin literature, like this deft demonstration from Seite et al. (at L’Oreal, which has a damn fine research division) that the ubiquitous enzyme lysozyme inhibits the breakdown of dermal elastin. Furthermore, UV exposure (a major source of photo-aging) stimulates lysozyme deposition in the skin, adding another layer to the body’s natural defenses against the ravages of solar radiation:

Cutaneous ageing, as a result of combined chronological and photo-ageing in sun-exposed areas, is accompanied by major modifications of the elastic fibres. … Our results indicate a reduction of elastin content with age in sun-protected and sun-exposed skin, associated for the latter with high elastin content, resulting in elastosis. Total UVA (320-400 nm), and in particular long wave UVA (UVA-1, 340-400 nm), induces lysozyme deposition in elastin fibres to a higher extent than solar simulated radiation (SSR, 280-400 nm). … In addition, a direct inhibitory effect of lysozyme on HLE was observed. Our data suggest that lysozyme prevents elastin degradation by HLE after binding to the damaged parts of the elastin network and by direct lysozyme-HLE interaction, which reduces HLE proteolytic activity. These observations contribute to a better understanding of the chronological and photo-induced changes of the dermal elastic network.

Far from being a peculiarity of the skin, this sort of mechanism might also be operating throughout the body: The extracellular matrix is chock full of collagens and elastins, and recent results from the cellular senescence field strongly suggest that aging cells secrete factors that degrade these structural proteins. Might protective factors be synthesized in response? The answer awaits experiments, but you heard it here, in a posting about skin, first.

If you’re as intrigued as I am, and interested in learning more about dermatological aging, Rabe et al. recently published a good comprehensive review:

Aging is a complex, multifactorial process resulting in several functional and esthetic changes in the skin. These changes result from intrinsic as well as extrinsic processes, such as ultraviolet radiation. Recent advances in skin biology have increased our understanding of skin homeostasis and the aging process, as well as the mechanisms by which ultraviolet radiation contributes to photoaging and cutaneous disease. These advances in skin biology have led to the development of a diversity of treatments aimed at preventing aging and rejuvenating the skin. The focus of this review is the mechanism of photoaging and the pathophysiology underlying the treatments specifically designed for its prevention and treatment.

(Hat tip to my dear friend Marc H for bringing that article to my attention.)

Learn, ponder, and enjoy — and in the meantime, remember: Wear sunscreen.