The fact that people who smoke develop wrinkles at an earlier age than their non-smoking counterparts seems to be due to an imbalance of extracellular matrix degrading enzymes and their respective inhibiting factors, according to an article in the Lancet (2001;357:935-6).
Researchers investigating the role of ultraviolet light on the expression of matrix metalloproteinase (MMP) enzymes in buttock skin of healthy volunteers incidentally found that this enzyme was already being expressed before ultraviolet exposure in some individuals, but not in others. Volunteers were retrospectively asked about their smoking status, and results indicated that smokers were more likely to express these enzymes than were non- smokers. There was no change in the expression of the known inhibiting factors between smokers and non-smokers.
The skin is a dynamic organ and depends on the deposition and remodelling of extracellular matrix proteins and terminal differentiation of basal cells into keratinocytes. Collagen accounts for more than 70% of the dry weight of skin, is the predominant protein of the extracellular matrix, and is degraded by these proteolytic MMP enzymes. MMPs are held in check by specific inhibitors, a relationship much like the proteinase-antiproteinase balance within the lung, which is deranged in individuals with a-1-antitrypsin deficiency, which manifests clinically as emphysema.
Increased expression of MMPs but not their inhibitors has been proposed to cause local degradation of collagens within the skin, resulting in loss of tone and eventually in wrinkles. Previous studies have shown the imbalance between MMPs and their inhibitors in response to sunlight, but this is the first report to show that smoking alters their equilibrium in vivo. Work published last year in the Archives of Dermatological Research (2000;292:18894) showed that human fibroblasts in vitro expressed MMPs in a dose dependent manner in response to increasing doses of water soluble extract from tobacco smoke.
While skin wrinkling is not an independent risk factor for increased morbidity or mortality on its own, this research may provide further data on how smoking mediates its other deleterious effects on individuals, and these findings could also be used in the fight against smoking.
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