Telomeres and cardiovascular disease
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
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
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
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.
More information about the Ageing