Our hearts are constantly pumping blood, and the human body naturally regulates that activity to make sure the same amount of blood flows in and out. Now, scientists have figured out the role a protein called titin plays in that regulatory process. Here’s what lead researcher Pieter de Tombe of Loyola said about the findings, published in PNAS.
How is the amount of blood going in and out of the heart regulated?
The amount it pumps varies a lot, between me talking to you and me going on a treadmill, and that amount is determined by a regulatory mechanism. But when that regulatory mechanism is broken, the pressure in your heart builds up. Then the pressure in your lungs builds up, your lungs fill with fluid, and that becomes congestive heart failure.
And what did you figure out about that regulatory mechanism?
If the muscle is a rubber band and you stretch it, it requires a force to do the stretching. … The elasticity of the [heart] muscle is really determined by a protein, titin. In heart failure, the titin is less stiff and becomes a bigger protein. In normal rat hearts with stiff titin, when we pull on the titin, we see some proteins in the heart muscle move to regulate the strength of the heart’s pump. In rats with short titin, we didn’t see it move.
What’s the application of that finding?
We don’t know exactly what the protein is, but we know that there’s a protein that’s being pulled on as titin is stretched. That’s the smoking gun to figure out what protein is the last step of this regulation — so we could target that protein to improve the length of it and bring the heart back to normal.
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