The finding may pave the way for development of new drugs to treat heart failure, which is a leading cause of death.
The study published in journal Circulation said that it is known that JP2 protein is important for normal functioning of the heart muscle membrane network called Transverse-tubules or T-tubules. "T-tubules help transmit electrical and chemical signals that make a heart-beat,'' said a university press release.
The university team studied microtubules, a network of fibers inside heart cells, in mouse models and found any high density of microtubules is always accompanied by abnormal localization of JP2 away from the T-tubule sites. There is instead a heavy concentration of JP2 to the periphery of the heart cell. "This abnormal distribution pattern is also seen in animal models of heart failure and in failing human heart muscle,'' it added.
The researchers also found that the drug colchicines decreases microtubule density and thus prevents the abnormal redistribution of JP2. The mouse is thus protected from heart failure.
"The findings suggest that colchicine could be considered as a treatment for patients with heart failure," said Long-Sheng Song, associate professor of internal medicine at the University of Iowa Carver College of Medicine. "The study also suggests that future approaches targeting junctophilin-2 directly might be a potential strategy for treating heart failure."
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