Medical Discovery News
What exactly causes a heart to fail? It may come down to a simple protein, which scientists recently identified as having an important role in how a heart goes from weakening to failing.
Your heart is a strong, muscular pump slightly larger than your fist that pushes blood through your body. Blood delivers the necessary oxygen and nutrients to all cells in all the organs. Every minute, your heart pumps five quarts of blood. Human hearts have four chambers: two atria on top and two ventricles on bottom. Oxygenated blood leaves the lungs, enters the left atrium, moves to the left ventricle, and is then pumped out of the heart to the rest of the body. After it circulates, blood returns to the heart, enters the right atrium, moves to the right ventricle, and is then sent back to the lungs for a fresh dose of oxygen. Although your heart beats 100,000 times each day, the four chambers must go through a series of highly organized contractions to accomplish this.
Any disruption of this process can have serious consequences such as heart failure, which is clinically defined as a chronic, progressive weakening of the heart’s ability to circulate enough blood to meet the body’s demands. To compensate, the heart enlarges, which increases contractions and the volume of blood pumped. Blood vessels elsewhere in the body narrow to keep blood pressure normal. Blood can even be diverted from less important organs, ensuring more vital organs like the brain and heart are satisfied. However, such responses mask the underlying problem: the weakening heart, which continues to worsen. Ultimately, the body can no longer compensate for the heart, which is when it will start to fail.
Scientists at the University of California, San Diego School of Medicine studied the cellular changes in weakened hearts to better understand the transition from the compensatory stage, when it works harder to pump blood, to the decompensation, when it fails to pump blood sufficiently. They were especially interested in a RNA-processing protein called RBFox2 because it is involved in the heart’s early development and its continuing functions. When genes are expressed, DNA is transcribed into RNA, which is then processed and eventually used to make proteins such as RBFox2.
Sure enough, levels of RBFox2 were dramatically reduced in the hearts of mice with a condition similar to heart failure. Then they genetically engineered mice without RBFox2, which developed symptoms of heart failure. Not only are low levels of this protein connected to weakened heart muscle, without enough of it the body cannot compensate and the heart declines more quickly. However, we still don’t know why levels of RBFox2 decline during the transition to the decompensatory phase of heart failure.
In the future, this research might be used to develop treatments that reverse the decline of RBFox2 and effectively slow or prevent heart failure.
Professors Norbert Herzog and David Niesel are biomedical scientists at the University of Texas Medical Branch. Learn more at medicaldiscoverynews.com.