 |
|
Telomerase and the Aging Cell
Implications for Human Health
Michael Fossel, MD, PhD
JAMA. 1998;279:1732-1735.
Recent research has shown that inserting a gene for the protein component of telomerase into senescent human cells reextends their telomeres to lengths typical of young cells, and the cells then display all the other identifiable characteristics of young, healthy cells. This advance not only suggests that telomeres are the central timing mechanism for cellular aging, but also demonstrates that such a mechanism can be reset, extending the replicative life span of such cells and resulting in markers of gene expression typical of "younger" (ie, early passage) cells without the hallmarks of malignant transformation. It is now possible to explore the fundamental cellular mechanisms underlying human aging, clarifying the role played by replicative senescence. By implication, we may soon be able to determine the extent to which the major causes of death and disability in aging populations in developed countries—cancer, atherosclerosis, osteoarthritis, macular degeneration, and Alzheimer dementia—are attributable to such fundamental mechanisms. If they are amenable to prevention or treatment by alteration of cellular senescence, the clinical implications have few historic precedents.
From the Department of Medicine, Michigan State University College of Human Medicine, East Lansing, and the College of Health Science, Grand Valley State University, Allendale, Mich.
THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES
The Maize Single myb histone 1 Gene, Smh1, Belongs to a Novel Gene Family and Encodes a Protein That Binds Telomere DNA Repeats in Vitro
Marian et al.
Plant Physiol. 2003;133:1336-1350.
ABSTRACT
| FULL TEXT
Atherosclerosis and Cancer: Common Molecular Pathways of Disease Development and Progression
ROSS et al.
Ann. N. Y. Acad. Sci. 2001;947:271-293.
ABSTRACT
| FULL TEXT
Studies of the molecular mechanisms in the regulation of telomerase activity
LIU
FASEB J. 1999;13:2091-2104.
ABSTRACT
| FULL TEXT
|
