[The role of incomplete terminal repair of chromosomal DNA in the aging of neurons and postmitotic organisms].
Incomplete repair of the DNA double helix terminus is an independent mechanism of the telomeric DNA shortening in non-dividing cells. This effect of incomplete terminal DNA repair may initiate aging of postmitotic neuroendocrine cells or even whole postmitotic organisms, if loss of the buffer telomeric DNA (due to incomplete terminal repair) is followed by the loss of significant information in the nucleotide sequences. We also consider a possibility of local aging of a cell group, e.g., in the locomotor system where extreme physical load favors accumulation of nuclear factors inducing accelerated shortening of telomeric DNA.
D000818:Animals; D016922:Cellular Senescence / Q000502:physiology; D002875:Chromosomes / Q000378:metabolism*; D004247:DNA / Q000096:biosynthesis*; D004260:DNA Repair / Q000502:physiology*; D008938:Mitosis / Q000502:physiology*; D009474:Neurons / Q000502:physiology*; D016615:Telomere / Q000502:physiology
D004247:DNA
O roli nepolmoĭ reparatsii kontsa khromosomnoĭ DNK v starenii neĭronov i postmitoticheskikh organizmov.