科普知识学英语研究人员发现导致心力衰竭的关键因素.docVIP

海量资料下载 免费学习英语 /xinlw.htm （申请网址） 洛基国际英语 竭诚为您服务 Some 5.8 million Americans suffer from heart failure, a currently incurable disease. But scientists at Temple University School of Medicines (TUSM) Center for Translational Medicine have discovered a key biochemical step underlying the condition that could aid the development of new drugs to treat and possibly prevent it. Drugs we currently use for heart failure are not very effective, explained lead investigator Walter J. Koch, PhD, Professor and Chairman of the Department of Pharmacology at TUSM, and Director of the Center for Translational Medicine at TUSM. But, he added, The more we learn about the disease mechanism, the more drug targets well find. ? That is what Koch and colleagues at Thomas Jefferson University and the University of California, Davis, achieved in their latest study, which appears in the March 5 issue of the online journal PLOS ONE. The report is the first to show that an enzyme called GRK5 (G-protein coupled receptor kinase 5) can gain access to a heart cells nucleus -- its command center, where control of its genes is maintained -- by way of a transport mechanism involving calcium and a protein known as?calmodulin（钙调蛋白）. Once calcium and calmodulin deliver GRK5 to the nucleus, the enzyme?usurps（夺取）?control over specific genes, ultimately causing hypertrophy, in which heart cells grow larger in size. Hypertrophy is a biological hallmark of heart failure. ? GRK5 had previously been identified as a key player in maladaptive cardiac hypertrophy, which is the end stage of heart failure, when the heart muscle becomes enlarged and unable to pump enough blood to keep vital organs functioning. While GRK5s ability to get inside the nucleus was known, Koch and colleagues worked to fill in the missing links in its transport mechanism. Those links, they hope, will not only allow them to better understand GRK5s role in causing heart cells to increase in size but also find ways to block that process to more