The role of telomeres in skin aging/photoaging.
Recent work has substantially elucidated the mechanisms of skin aging and photoaging. In particular, a central role for telomere-based signaling can be inferred. Intrinsic aging is largely controlled by progressive telomere shortening, compounded by low grade oxidative damage to telomeres and other cellular constituents, the consequence of aerobic cellular metabolism. In sun exposed skin, UV irradiation also damages DNA and accelerates telomere shortening. Aging and photodamage appear to share a common final pathway that involves signaling through p53 following disruption of the telomere. These telomere-initiated responses, in combination with UV-induced damage to critical regulatory genes, lead to the familiar picture of "photoaging." These and other insights into the molecular basis for skin aging/photoaging may lead to enhanced management options.
Kosmadaki
M G
MG
Department of Dermatology, Boston University School of Medicine, 609 Albany Street, Boston, MA 02118-2394, USA.
Gilchrest
B A
BA
D017209:Apoptosis; D002455:Cell Division; D016922:Cellular Senescence / Q000502:physiology; D004247:DNA / Q000528:radiation effects; D004249:DNA Damage; D006801:Humans; D018384:Oxidative Stress; D012867:Skin / Q000528:radiation effects / Q000648:ultrastructure*; D015595:Skin Aging / Q000473:pathology*; D013472:Sunlight / Q000009:adverse effects; D020080:Tandem Repeat Sequences; D019098:Telomerase / Q000502:physiology; D016615:Telomere / Q000502:physiology* / Q000648:ultrastructure; D035341:Telomeric Repeat Binding Protein 2 / Q000502:physiology
D035341:Telomeric Repeat Binding Protein 2; D004247:DNA; D019098:Telomerase