The discovery is expected to benefit those who will need heart coronary bypass surgery, an angioplasty - the mechanical widening of a narrowed or totally blocked blood vessel - or will undergo haemodialysis.

Professor Levon Khachigian, from UNSW ™s Centre for Vascular Research, who previously pioneered "molecular assassin" drug technology, describes this novel mechanism he discovered as a molecular dictatorship with a conscience".

"The dictator is a specific gene suppressor called YY1, which has the therapeutically appealing capacity to differentiate between certain cell types when it goes about its activity," said Professor Khachigian.

This key finding has just been published in the world's premier cardiovascular research journal, Circulation Research.

Professor Khachigian's research provides new hope in tackling the global problems of coronary bypass graft failure, and restenosis - the closing or narrowing of an artery that was previously opened by a procedure such as angioplasty.

"While the most effective way to head off restenosis is a drug-coated stent, the drugs that sit on these stents inhibit the growth of good cells as well as the bad."

If you had to have catheter intervention to re-open an occluded artery, for sustained symptom-free benefit you would be hoping for suppressed smooth muscle cell growth, without affecting endothelial cell growth, says Professor Khachigian.

And that ™s exactly what happens when we simply top up blood vessels with the body ™s natural reserves of YY1."

Professor Khachigian is seeking commercial partnerships that can apply this technology in the clinic.

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The markedly reduced expression (or down-regulation) of genes involved in chromatin remodeling, an ,epigenetic, regulator of gene expression, suggested that transcriptional activity might be dysregulated across the genome.

Though the dominant model attributes the physical effects of aging to an accretion of isolated genetic insults, these results link age-related decline to global mechanisms operating across the genome. In the researchers ,epigenetic view of aging," chromatin dysregulation provides a logical explanation for the numerous and diverse age-related changes observed at the molecular, cellular, and organismal levels. Over the normal course of aging, chromatin dysregulation leads to dysregulation of many genes, which in turn leads to a loss of normal cellular functions and a loss of growth regulation. These changes ultimately increase the risk of cancer, which, in many of its forms, increases dramatically with age. Future studies can investigate how epigenetic regulation, inflammation, and the stress response interact to better understand the molecular mechanisms of aging, and why so many of us face a high risk of cancer in our later years.

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