主页 > 医学新闻 >
【bio-news】突变诱导良药---自然突变让心衰患者受
By Kelli Whitlock Burton
ScienceNOW Daily News
21 April 2008
Scientists have discovered a genetic mutation that might extend the lives of many African Americans after heart failure by mimicking a common class of drugs called beta blockers. The findings could explain why clinical trials of the drugs have shown little benefit to African-American patients.
The heart doesn't stop beating during heart failure. Instead, it stops pumping blood efficiently. The condition can be caused by a number of diseases--including diabetes and hypertension--that keep the heart from filling with blood or decrease blood flow from the heart to the rest of the body. As the heart falters, the body releases adrenaline to keep the organ pumping. Too much adrenaline overworks the heart, and eventually the organ gives out.
Beta blockers halt this process by blocking adrenaline receptors and slowing the heart rate. However, studies suggest that the drugs don't work in many African Americans. To figure out why, researchers at the University of Maryland, Baltimore, and Washington University in St. Louis, Missouri, took a close look at GRK5, one of the receptor proteins in the heart that responds to adrenaline. After sequencing DNA from 96 heart-failure patients, the team found that 40% of African Americans in the study had a mutation in GRK5. Only 2% to 3% of participants of European or Chinese descent had this variant, called Leu41.
The researchers then followed 375 other African-American heart-failure patients with and without the mutation until they died or received a heart transplant, an average period of 30 months. Some patients took beta blockers and some didn't. Of those who did, patients with Leu41 had the same survival rate as those without the mutation. The surprising finding, however, was that among patients who didn't take the drugs, those with Leu41 lived almost twice as long as those without the mutation. Reporting online this week in Nature Medicine, the team says it believes the mutation mimics beta blockers, slowing heart rate by blocking GRK5's ability to respond to adrenaline.
"This work suggests that the reason it's been hard to demonstrate a benefit [of beta blockers] in African Americans is that almost half of them are already getting the benefit naturally,?says David Kass, a cardiologist at Johns Hopkins University in Baltimore, Maryland, who was not part of the study. But that doesn't mean that beta blockers are useless for patients with Leu41, says Gerald Dorn, a senior author of the study and a cardiologist at Washington University School of Medicine. Beta blockers work against several different types of heart disease, so "I'm not willing to say that having the protective gene is equal in every way to beta-blocker therapy." 本人已认领该文编译,48小时后若未提交译文,请其他战友自由认领。 Mutation Makes Good Medicine
突变诱导良药
By Kelli Whitlock Burton
ScienceNOW Daily News
21 April 2008
Scientists have discovered a genetic mutation that might extend the lives of many African Americans after heart failure by
mimicking a common class of drugs called beta blockers.
科学家发现许多非洲裔美国人存在一种基因突变,他能模拟beta-受体阻断剂这种常见的心血管药物,可能有助于延长心衰患者的生命。
The findings could explain why clinical trials of the drugs have shown little benefit to African-American patients.
此发现能解释为什么药物在临床试验中对非洲裔美国病人收效甚微的现象。
The heart doesn't stop beating during heart failure. Instead, it stops pumping blood efficiently.
心衰病人的心脏并没有停止跳动,而是不能有效的泵血。
The condition can be caused by a number of diseases--including diabetes and hypertension--that keep the heart from filling
with blood or decrease blood flow from the heart to the rest of the body.
很多疾病都能引起心衰,促使心脏血容量增高或是心排出量减少而引起心功能不全,其中包括糖尿病和高血压。
As the heart falters, the body releases adrenaline to keep the organ pumping. Too much adrenaline overworks the heart, and
eventually the organ gives out.
例如心颤患者,体内释放的肾腺上素能保持心脏收缩力。但过多的肾腺上素作用于心脏就会引起心率失常,导致室颤。
Beta blockers halt this process by blocking adrenaline receptors and slowing the heart rate.
beta-受体阻断剂通过阻断肾上腺素受体而阻断肾上腺素的这种正性肌力作用,减缓心率。
However, studies suggest that the drugs don't work in many African Americans.
但是,大量研究发现这种药物对很多非洲裔美国人却不起作用。
To figure out why, researchers at the University of Maryland, Baltimore, and Washington University in St. Louis, Missouri,
took a close look at GRK5, one of the receptor proteins in the heart that responds to adrenaline.
阅读本文的人还阅读:
作者:admin@医学,生命科学 2010-10-17 17:11
医学,生命科学网