Telomeres and cardiovascular disease

Thomas Mahoney excelife at earthlink.net
Mon Mar 8 20:09:11 EST 1999


We have been discussing the effects of telomeric shortening on aging and age 
related diseases.

One item under discussion is the effects of telomeric shortening on the 
cardio-vascular system and it has been suggested that readers of the groups 
specializing in these areas could have some valuable input on this 
discussion.

In 1995 Dr. Harley of Geron Corp. suggested, (in; Proc Natl Acad Sci U S A 
1995 Nov 21;92(24):11190-11194 "Telomere length and replicative aging in 
human vascular tissues.", Chang E, Harley CB), that there was a "higher
hemodynamic stress and increased cell turnover in arteries...consistent with 
a role for focal replicative senescence in cardiovascular diseases."

Additional research, (Virchows Arch 1997 Feb;430(2):155-162, "Declining 
density of intimal smooth muscle cells as a precondition for atheronecrosis 
in the coronary artery.", Tracy RE) has shown that "Aging produces 
atheronecrosis through effects that are associated with diminishing cell 
density" and further, (Circ Res 1998 Apr 6;82(6):704-712 "Cooperative 
interactions between RB and p53 regulate cell proliferation, cell senescence, 
and apoptosis in human vascular smooth muscle cells from atherosclerotic 
plaques.", Bennett MR, et al), that human plaque VSMCs have slower rates of 
cell proliferation and earlier senescence than do cells from normal 
vessels... and high level of apoptosis".

The work of Dr. H. Vaziri including, (Exp Gerontol 1996 Jan;31(1-2):295-301 
"From telomere loss to p53 induction and activation of a DNA-damage pathway
at senescence: the telomere loss/DNA damage model of cell aging.", Vaziri H, 
Benchimol S) and (Biochemistry (Mosc) 1997 Nov;62(11):1306-1310 "Critical 
telomere shortening regulated by the ataxia-telangiectasia gene acts as a DNA 
damage signal leading to activation of p53 protein and limited life-span of 
human diploid fibroblasts. A review.", Vaziri H), suggests that "It is the 
consequence of telomere loss...that leads to...the eventual G1 block of 
senescence."

Given this research it has been suggested that telomeric lengthening therapy, 
possibly through the introduction of hTRT to activate the enzyme telomerase, 
in the cells under stress in the vascular system could have the effect of 
avoiding the cellular loss associated with plaque formation.

Comments, criticisms, or analysis? 



Thomas Mahoney, Pres.
Lifeline Laboratories, Inc.
http://home.earthlink.net/~excelife/index.html






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