Photoageing
Premature skin ageing caused by cumulative UV radiation exposure, characterised by wrinkles, pigmentation changes, loss of elasticity, and rough texture. Photoageing is distinct from intrinsic (chronological) ageing and is the primary driver of visible skin deterioration. UV protection is the most effective prevention strategy.
Technical Context
Photoageing (extrinsic ageing) results from cumulative UV exposure: UVB (290-320nm) causes direct DNA damage (cyclobutane pyrimidine dimers, 6-4 photoproducts), while UVA (320-400nm) generates ROS that cause indirect DNA damage, lipid peroxidation, and protein modification. Chronic UV exposure → persistent MMP induction (MMP-1, -3, -9 degrading collagen and elastin), reduced procollagen synthesis (UV-activated AP-1 transcription factor inhibits type I collagen gene expression), solar elastosis (accumulation of degraded, tangled elastic fibres — the histological hallmark of photoageing), and melanocyte irregularity (lentigines/age spots). Clinically: wrinkles, rough texture, dyspigmentation, telangiectasia, and loss of elasticity. Photoageing can be partially prevented (sun protection) and partially treated (retinoids, which stimulate collagen synthesis and normalise cell turnover). Peptide-based anti-photoageing strategies target: collagen stimulation, MMP inhibition, antioxidant protection, and melanocyte regulation.