Washington, Sept. 19: Scientists at the Texas A&M Health Science Center Institute of Biosciences and Technology at Houston have discovered what causes the slow death of heart cells to occur, thus leading to heart failure.
By identifying the key factor in a mouse model, the scientists are now hopeful that it will be successful against hypertension and erectile dysfunction.
Robert Schwartz, Ph.D., interim director of HSC-IBT and co-senior author said that the team of researchers had found a new drug that may be successful in not only blocking heart failure, but also stopping pulmonary hypertension, vascular hypertension and erectile dysfunction.
“We found a new drug target that may block the onset of human heart failure and may also be effective against pulmonary hypertension, vascular hypertension and erectile dysfunction,” he said.
The human genome contains about 500 to 1,000 protein kinase genes that regulate many aspects controlling cell growth, movement and even cell death.
ROCK-1, a protein kinase, is super-activated following its cleavage (split) with a caspase, an enzyme involved in the death of heart cells in a process called “apoptosis,” or programmed cell death.
The researchers, in their study of ROCK-1 in mice, found that triggering apoptosis is essential in the programmed death of heart muscle cells, and that once it is removed, heart failure and related diseases could someday be reduced.
“Once the process begins, it gathers speed, like a snowball rolling downhill. Consequently, by inhibiting or removing ROCK-1 through therapeutics, heart failure and related diseases could someday be reduced. The therapeutic potential of these observations is attractive because inhibition of ROCK-1 appears relatively safe,” Dr. Schwartz said.
Mark Entman, M.D., professor at the Baylor College of Medicine said that the study had proven that ROCK-1 activation “promotes” the death of heart cells.
“Our study demonstrates that ROCK-1 activation promotes cardiac cell death and is also activated by programmed cell death pathways,” he said.
Michael Schneider, M.D., professor at the Baylor College of Medicine said that though at the present moment there is no drug tailor-made for ROCK-1, the study showed the need for one.
“Currently, there is no drug specific for ROCK-1 and other ROCK-like kinases. But, our report should drive interest in developing a selective ROCK-1 inhibitor,” he said.
The study is currently available online in the Proceedings of the National Academy of Sciences, and will be made available in print in an upcoming issue in the journal. (ANI)