As the belt in your old favorite pajamas, overworked hearts often lose their elasticity and ability to effectively pump blood - a condition called congestive heart failure. Tired hearts are prone to arrhythmias that cause sudden death. Now, researchers reporting in tomorrow's issue of the Journal Cell found a domestic signaling causing a closely related form of heart failure in mice. The discovery could lead to new drugs to maintain the stressed hearts of sagging.
Hearts attempt to compensate for the abnormal stress on their walls by increasingly large. This works for a while, but eventually the muscle cells get long and thin, and they fail as elastic stretched. fibrous deposits also form and can cause strokes and arrhythmic death. Scientists have long suspected that calcium in heart cells could play a role in this tragic transformation. Then Eric Olson, a biologist at the University of Texas Southwestern Medical Center in Dallas and colleagues were excited when they found a protein called calcium regulating NF-AT3 which seemed to also turn on genes that caused the widening heart.
To see if NF-AT3 could cause heart failure by itself, the researchers created mice that have an enzyme that has kept active NF-AT3 way, whatever the level of calcium . To the surprise of satisfaction group, mice "recapitulate all physiological and pathological aspects of human heart failure," said Olson, including the fibrous growth, arrhythmia, and sudden death.
The researchers warn that there may be other mechanisms that cause hearts to grow and fail in humans, but many are optimistic the finding may lead to new drug treatments. Indeed, the Olsen group gave the even mutant mice immunosuppressive drug (cyclosporine) to block NF-AT3 activity and found that it kept them healthy. Because the way seems specific to the heart, it could also be used to develop drugs for the heart with few side effects, said Stanford University Medical Center researcher Jerry Crabtree. "I would be very surprised if a pharmaceutical company did not jump immediately on this issue."
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