Statins Can Prevent Premature Ageing Of Arteries

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Main Category: Statins
Also Included In: Cardiovascular / Cardiology;  Stroke;  Seniors / Aging
Article Date: 29 Sep 2008 - 8:00 PDT

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New research from the UK found that statins, normally prescribed for lowering cholesterol and reducing heart attack risk, can stop arteries ageing prematurely in patients with advanced heart disease.

The study is published in the 26 September issue of the the journal Circulation Research and is the work of Professor Martin Bennett, British Heart Foundation (BHF) Professor of Cardiovascular Sciences at Cambridge University and colleagues from the Division of Cardiovascular Medicine also at Cambridge. BHF also funded the research.

Bennett said:

"It is an exciting breakthrough to find that statins not only lower cholesterol but also rev-up the cells' own DNA repair kit, slowing the ageing process of the diseased artery."

Cells in the human body can only divide and replicate a limited number of times. The more divisions cells undergo, the older the tissue, and the higher the risk of damaged DNA due to the shortening of telomeres (bits of non-functional DNA on the ends of genes that protect against transcription errors), which gradually outstrips DNA repair.

The cells in the arteries of people with heart disease divide between 7 and 13 times faster than normal, resulting in a premature accumulation of older cells that do no divide efficiently and an even faster rate of outstripping the DNA repair process.

The result is premature ageing of arterial tissue which is less efficient at taking care of itself, including not being so good at stopping fatty deposits or atherosclerotic plaques from sticking to artery walls and narrowing them, so they eventually get blocked and cause a heart attack or a stroke.

The BHF team at Cambridge had already found that patients in advanced stages of heart disease had arteries that were biologically up to 40 years older than actual age because of DNA damage. They also knew that statins could reduce DNA damage in cells in the test tube, but the underlying mechanism was still a mystery.

Bennett and colleagues found that statins increased the levels of Nijmegen breakage syndrome (NBS)-1 protein which with another protein called human double minute protein Hdm2, is essential for, and can also speed up, DNA repair. The researchers found that statins did not reduce DNA damage through oxidative stress, and that the main way they slowed down artery cell ageing and loss of telomeres was by activating a "novel mechanism of accelerating DNA repair, dependent on NBS-1 stabilization and Hdm2."

From this they concluded that:

"Statin treatment may delay cell senescence [ageing] and promote DNA repair in atherosclerosis."

Bennett commented that:

"The major risk factors that cause heart disease - high blood pressure, diabetes, high cholesterol, smoking, lack of exercise and poor diet - all speed up a final common cellular ageing process, which is irreversible. Reducing your risk through lifestyle changes can help to prevent this - and we've found that statins may also lend a hand."

"If statins can also do this in other cells, they may protect normal tissues from DNA damage that occurs as part of chemotherapy and radiotherapy for cancer, potentially reducing the side effects associated with these treatments," he added.

Professor Peter Weissberg, Medical Director at the BHF said:

"Too much cholesterol in the blood induces a repeated cycle of damage and repair in the blood vessel wall which results in a heart attack if the repair mechanism is inadequate. Statins protect against heart attacks by reducing cholesterol levels and subsequent damage to the vessel wall."

"This research has shown that they may also enhance the blood vessels' natural repair mechanisms. Fundamental research of this nature is essential if we are to understand the cellular mechanisms that cause heart attacks and develop new treatments to prevent what still remains the biggest cause of death and disability in our society."

"Statins Use a Novel Nijmegen Breakage Syndrome-1-Dependent Pathway to Accelerate DNA Repair in Vascular Smooth Muscle Cells."
Melli Mahmoudi, Isabelle Gorenne, John Mercer, Nicola Figg, Trevor Littlewood, and Martin Bennett
Circ Res., Volume 103, Issue 7; September 26, 2008, pp 717-725.
DOI:10.1161/CIRCRESAHA.108.182899

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Written by: Catharine Paddock, PhD


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