Targeted drug therapy for cardiac health soonPublished On: Mon, Dec 29th, 2014 | Cardiovascular / Cardiology | By BioNews
Researchers have discovered that a new set of proteins called ion channels can help doctors develop new drugs for people suffering from cardiac arrhythmia or irregular heartbeat .
They found that ion channels generate the electrical signals of the heart differently than previously thought.
Proteins called ion channels generate the electrical signals of the heart by opening a gate or pore for charged ions to cross the cell membrane.
It is like if the ion channels are the musicians of an orchestra, the membrane voltage is the conductor.
That is, the membrane voltage signals to the channels the proper time to open and keeps them all in rhythm.
For one important channel in the heart, called KCNQ1, the membrane voltage not only causes the channel to open, but also determines the properties of the electrical signals – acting as both conductor and composer rather than only conductor as previously believed, the findings showed.
“This knowledge we are providing is to revise the model built in the 1950s,” said Jianmin Cui, professor of biomedical engineering at Washington University in St. Louis.
KCNQ1 is so important to the heart’s rhythm that there are more than 250 mutations of the channel that have been associated with cardiac arrhythmia, Cui added.
“The trouble was that without an accurate model of how the channel gating works, we were limited in our understanding of why these mutations lead to fatal arrhythmias and in our ability to design therapeutic interventions that can specifically fix the defect in the afflicted tissues,” he noted.
This discovery could lead to new drug therapy for the disorder, the researchers pointed out in a paper that appeared in the journal eLife.
Zaydman, M, Kasimova M, McFarland K, Beller Z, Hou P, Kinser H, Liang H, Zhang G, Shi J, Tarek M, and Cui J. Domain-domain interactions determine the gating, permeation, pharmacology, and submit modulation of the IKs ion channel. eLife, Dec. 23, 2014.