Search results
Results from the WOW.Com Content Network
Many life span influencing genes affect the rate of DNA damage or DNA repair. Genetics of aging is generally concerned with life extension associated with genetic alterations, rather than with accelerated aging diseases leading to reduction in lifespan. The first mutation found to increase longevity in an animal was the age-1 gene in ...
[18] [19] Mouse cells that are deficient for maturation of prelamin A have increased DNA damage and chromosome aberrations, and show increased sensitivity to DNA damaging agents. [20] In progeria , the inadequacy of DNA repair, due to defective LMNA, may cause features of premature aging (see DNA damage theory of aging ).
Other form of age-associated changes in gene expression is increased transcriptional variability, that was found first in a selected panel of genes in heart cells [26] and, more recently, in the whole transcriptomes of immune cells, [27] and human pancreas cells. [28]
Antagonistic pleiotropy on the other hand deals with one gene that creates two traits with one being beneficial and the other detrimental. In essence, this refers to genes that offer benefits early in life, but later accumulate a cost. [1] In other words, antagonistic pleiotropy is when the resultant relationship between two traits is negative.
Chronic inflammation due to SASP from senescent cells can also reduce the capacity of the immune system to remove senescent cells. [66] T cells, B cells, and NK cells have all been reported to become senescent themselves. [68] Senescent-like aging CD8+ cytotoxic T-lymphocytes become more innate in structure and function, resembling NK cells. [69]
Gene expression is imperfectly controlled, and it is possible that random fluctuations in the expression levels of many genes contribute to the aging process as suggested by a study of such genes in yeast. [70] Individual cells, which are genetically identical, nonetheless can have substantially different responses to outside stimuli, and ...
Senescent cells are highly metabolically active, producing large amounts of SASP, which is why senescent cells consisting of only 2% or 3% of tissue cells can be a major cause of aging-associated diseases. [32] SASP factors cause non-senescent cells to become senescent. [39] [40] [41] SASP factors induce insulin resistance. [42]
In older cells, however, the same genes nucleosome loss at the promoter is more prevalent which leads to higher transcription of these genes. [10] This phenomenon is not only seen in yeast, but has also been seen in aging worms, during aging of human diploid primary fibroblasts, and in senescent human cells.