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Scientists make key heart and kidney discoveries

29/04/2008

Scientists say they have made two key discoveries that could help develop treatments for heart and kidney problems.

The researchers found a gene that can cause the heart to become enlarged, which greatly increases the risk of heart attacks and heart failure.

A second study also discovered a gene that can cause the kidney to become inflamed, increasing the risk of kidney failure.

The two studies, published in the journal Nature Genetics, say they could help scientists understand the conditions and open up further routes for them.

In the first study, scientists at Imperial College London (ICL) and the Medical Research Council (MRC) found that a gene called osteoglycin (Ogn), which had not previously been linked with heart function, plays a key role in regulating heart growth.

They say their discovery suggests that the gene can behave abnormally in some people and that this can lead to the heart becoming abnormally enlarged.

"A person whose heart is enlarged is more likely to suffer a heart attack or heart failure than someone whose heart is a normal size," said Dr Stuart Cook, one of the corresponding authors of the study from the MRC Clinical Sciences Centre and the National Heart and Lung Institute at ICL.

"We can't currently treat the condition directly, so lowering a patient's blood pressure is the only option we have. Now that we are unravelling how genes control heart growth, we can gain a better understanding of common forms of heart disease. This should lead to new and more effective ways of treating people."

The second study found that the gene Jund controls the activity of a group of cells thought to be responsible for potentially severe inflammation of the kidney.

Scientists at Imperial College London say the gene could offer a route for tackling the auto-immune destruction of kidney tissue which can occur in lupus patients, causing renal failure.

"We are hoping that this discovery will allow us to find a new and effective way of treating this potentially fatal form of kidney failure," said Professor Tim Aitman.

"By reducing the activity of the Jund gene, we were able to reduce activity of inflammatory cells that can become overactive in certain diseases of the kidney.

"Such a therapy would be of obvious benefit to patients suffering from auto-immune diseases such as lupus. This would allow them to avoid dialysis and maintain their quality of life."