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揭密心臟肥大基因 / 英國醫學研究委員會 (2011)

Posted by HP 
揭密心臟肥大基因 / 英國醫學研究委員會 (2011)

分類標籤: 醫學

資料來源:英國醫學研究委員會 2011年10月5日




研究人員解釋,不正常的Endog基因會干擾心肌細胞能量工廠『粒線體』(mitochondrion)的正常運作,導致細胞無法製造足夠能量供應心臟運轉所需,心肌細胞為了彌補能量不足而必須加倍工作,加工過程中產生有毒副產物『反應性含氧物種』(reactive oxidative species,ROS),刺激心臟肌肉增長,造成心臟肥大,影響心臟功能。



New research found a genetic link for a “heavy heart”
(From the Medical Research Council, 5th Oct. 2011)

An international research team with joint forces from Europe, the US and Japan, led by the Medical Research Council (MRC) in the UK, has for the first time pinpointed a single gene - Endog gene - associated with one of the leading causes of heart thickening and failure.

Scientists have found that the Endog gene in rats and mice influences the thickness of the muscular heart wall, how well the heart pumps and how much fat accumulates inside the organ. It is believed that the findings bring the researchers one step closer to developing new treatments that target the underlying causes of heart conditions, rather than just treating the symptoms.

Enlargement of the heart is one of the many causes of heart problems. It doesn’t only have serious impacts on people’s daily life but also cause heart muscle to turn weak or stiff or become damaged, hence affecting the heart’s ability in pumping blood, resulting in heart failure at the end. While some cases of enlarged heart are caused by other medical conditions, such as diabetes or high blood pressure, a person’s genetic makeup can also play an important role. Previous studies have shown a link between heart wall thickening (cardiac hypertrophy) and several sections of the genetic code, but this is the first time researchers have isolated a single gene.

Researchers explained that malfunctioned Endog gene interferes the heart cells’ energy source – the mitochondria. Like any other muscle in our body, the heart needs energy to keep in pumping. If the mitochondria don’t work properly, the heart struggles to make enough energy and the cells produce toxic by-products, called reactive oxidative species, which increase thickening of the heart wall.

It was previously thought that the Endog gene was involved in cell death. This new research surprisingly unveiled its connection to the mitochondria and the enlargement of the heart, showing scientists a completely different angle to explore heart problems. It opens new ways to develop treatments which target the mitochondria and toxic oxidative molecules.

Edited 4 time(s). Last edit at 12/07/2011 03:11AM by HP.