On the horizon: DNA 'caps' offer target for heart drugs
Telomeres — tiny caps that protect the ends of chromosomes — were the focus of the 2009 Nobel Prize in Physiology or Medicine, which was shared by Elizabeth H. Blackburn of the University of California, San Francisco, Carol W. Greider of Johns Hopkins, and Harvard's Jack W. Szostak. Telomeres contain a unique sequence of DNA that protects chromosomes from unraveling and being broken apart, which would be catastrophic for cells. As cells age, telomeres shorten. But high activity of telomerase, a telomere-making enzyme, can stave off cell aging and decline. The discovery that telomeres act like biological clocks that tick off the years could someday influence the treatment of atherosclerosis, heart failure, and other cardiovascular conditions.
Several research groups have shown that people with cholesterol-clogged coronary arteries, victims of heart attacks, and those with heart failure have shorter telomeres than healthy people. It is possible that some people are born with shorter telomeres, predisposing them to cardiovascular disease as their heart and blood vessel cells age more quickly. It is also possible that shorter telomeres are a consequence of inflammation and other processes that cause cardiovascular disease.
Even before cause and effect have been established, the hunt is on for drugs or therapies that can protect telomeres, and thus keep heart and blood vessel cells young and strong. One study has shown that statins may do this. Others are looking at the possibility of using drugs or gene therapy to increase the activity of telomerase and thus protect these structures. Such therapies would be unexpected fruits of the Nobel Prize winners' work.