Targeting the age-related occurrence, removal, and accumulation of molecular damage by hormesis.
Strategies for testing and developing effective means of intervention, prevention, and modulation of aging incorporate means to minimize the occurrence and accumulation of molecular damage, to reduce molecular heterogeneity, and to evaluate the relevance of the type and extent of damage with respect to its role in aging and age-related diseases. One such approach is that of mild stress-induced hormesis, which stimulates maintenance and repair systems and strengthens the homeodynamic space of cells and organisms. Hormesis through mild heat shock, natural and synthetic hormetins, and other stressors brings about several antiaging effects in human fibroblasts, keratinocytes, and telomerase-immortalized bone marrow stem cells. Depending on the cell type, these antiaging hormetic effects include extension of replicative life span, enhanced proteasomal activities, increased chaperone levels, and improved wound healing, angiogenesis, and differentiation. The main molecular pathways for achieving such hormetic effects are through targeting the processes for the repair and removal of molecular damage, which can slow aging.
Rattan
Suresh I S
SI
Laboratory of Cellular Ageing, Department of Molecular Biology, Aarhus University, Aarhus, Denmark.
D000375:Aging / Q000502:physiology*; D005347:Fibroblasts / Q000166:cytology / Q000378:metabolism*; D018869:Heat-Shock Response / Q000502:physiology*; D006801:Humans; D015603:Keratinocytes / Q000378:metabolism*; D008017:Life Expectancy; D046988:Proteasome Endopeptidase Complex / Q000378:metabolism; D014945:Wound Healing
D046988:Proteasome Endopeptidase Complex