Mitotic misregulation and human aging.

  title={Mitotic misregulation and human aging.},
  author={Danith H. Ly and David J. Lockhart and Richard A. Lerner and Peter G. Schultz},
  volume={287 5462},
Messenger RNA levels were measured in actively dividing fibroblasts isolated from young, middle-age, and old-age humans and humans with progeria, a rare genetic disorder characterized by accelerated aging. Genes whose expression is associated with age-related phenotypes and diseases were identified. The data also suggest that an underlying mechanism of the aging process involves increasing errors in the mitotic machinery of dividing cells in the postreproductive stage of life. We propose that… 

Transcripts of aging.

Molecular basis of mitotic decline during human aging

Modulation of mitotic efficiency through FoxM1 is proposed as a potential strategy against aging and progeria syndromes by preventing aneuploidy and ameliorating cellular phenotypes associated with aging.

Aging and nuclear organization: lamins and progeria.

FoxM1 repression during human aging leads to mitotic decline and aneuploidy-driven full senescence

In aged cells, mitotic gene repression leads to increased chromosome mis-segregation and aneuploidy that triggers permanent cell cycle arrest and full senescence, and modulation of mitotic efficiency through FoxM1 is proposed as a potential strategy against aging and progeria syndromes.

Genome-wide study of aging and oxidative stress response in Drosophila melanogaster.

It is suggested that free radicals play an important role in regulating transcript levels in aging but that they are not the only factors.

Mitotic Dysfunction Associated with Aging Hallmarks.

Based on the evidence, a mutual causality between aging and aneuploidy is proposed, and modulation of mitotic fidelity is suggested as a potential means to ameliorate healthy lifespan.

Towards restoring proper chromosome segregation and preventing ageing

A link between ageing and the erroneous assembly of the apparatus required for a proper cellular division is shown and a strategy to delay age‐related CIN is described.

p53 and a human premature ageing disorder


Replicative Senescence: Implications for in Vivo Aging and Tumor Suppression

Normal cells have limited proliferative potential in culture, a fact that has been the basis of their use as a model for replicative senescence for many years, and results indicate that multiple levels of control contribute to the irreversible growth arrest.

Progeria: a human-disease model of accelerated aging.

    W. Brown
    Biology, Medicine
    The American journal of clinical nutrition
  • 1992
It is hypothesize that the failure of patients with progeria to thrive may be due to a bioinactive form of GH and a lack of vasculogenesis caused by excess HA, a key gene with a major effect on normal aging.

Gene expression profile of aging and its retardation by caloric restriction.

Transcriptional patterns of calorie-restricted animals suggest that caloric restriction retards the aging process by causing a metabolic shift toward increased protein turnover and decreased macromolecular damage.

Relationship between donor age and the replicative lifespan of human cells in culture: a reevaluation.

The results clearly indicate that, if health status and biopsy conditions are controlled, the replicative lifespan of fibroblasts in culture does not correlate with donor age.

Polo kinase: the choreographer of the mitotic stage?

The extension of identity beyond the catalytic domain strongly suggests that members of another conserved serine/threonine kinase family appears to be able to control the dynamics of cellular architecture and whether the polo-like kinases of different organisms have equivalent biological functions.