The micro-inflammatory theory of skin ageing: Mechanisms and possible interventions
Fighting skin aging can be considered in the frame of the micro-inflammatory hypothesis, a cyclic mechanism, which can be tackled step by step. Damaged cells release pro-inflammatory signals inducing mast cells to secrete histamine and TNF-a (Tumor Necrosis Factor a). Endothelial cells in blood vessels synthesize I-CAM 1 (Inter-cellular Adhesion Molecule 1), a signal for immune cells to release H2O2 and exit the vessels. Immune cells follow chemotactic signals and fray a path damaging the dermis. In the absence of chemotactic signals, immune cells damage the connective tissue surrounding the blood vessels. When damaged cells are reached, immune cells release an oxidative burst, engulf cellular debris and proceed to the lymphatic system. Innocent bystander cells can be damaged, thus triggering another round of release of pro-inflammatory signals. The accumulation of damage provoked by this process can be hindered by the appropriate topical application of anti-oxidants such as Vitamins C and E, of stimulators of DNA repair and booster of ATP synthesis such as nicotinamide. Aminoguannidine and T. chebula extracts prevent pro-inflammatory glycation and other interventions against dry skin or age spots are discussed.
The expression “damage of aging” is a very evocative yet a very misleading expression. As a matter of fact, it was pointed out by the collective work of the European Network for the Biology of Aging in the late 1990s (1), that aging is essentially the consequence, not the cause, of damage. From a biochemical, quantitative point of view, aging can be defined as the accumulation of molecular damage (2). Molecular damage and remodeling can impair the organization of molecules in the extracellular matrix, or the basic physiology of a cell, with unwanted consequences.
Macroscopic signs of skin aging such as sagging, wrinkles, age spots, varicose veins, spider veins, loss of elasticity, elastotic skin, cutis rhomboidalis, dullness, loss of radiance and of luminosity are the consequence of causes as diverse as solar exposure, anoxia, wounds, infections, physical strain, psychological stress, cigarette smoking, protein glycation and the drinking of alcoholic beverages.
One of the questions tackled by the European Network for the Biology of Aging was “Do these factors of skin aging share common mechanistic features?” and the answer was ...