As a possible treatment for such conditions as congestive heart failure, this technique could present an alternative to current therapies that counteract heart muscle weakness by boosting cellular calcium content, Shroff said. The heightened calcium improves muscle contraction but also results in more energy consumption in hearts that often are energy-starved to begin with.
In contrast, inhibiting HDAC alters a natural process to make heart muscle more sensitive to the prevailing level of calcium, he said.
We did not create this processwe are just manipulating what is already there, Shroff explained. The physiology to block HDAC is already there, and we just took advantage of that. This perturbation does not require greater mobilization of calcium, so we wont end up with increased cardiac energy consumption. Thats been the Achilles heel of treatment so far.
The teams next step involves examining HAT- and HDAC-driven regulation of cardiac contraction in the whole animal rather than just muscle samples. Then it can better determine the overall significance of the newly discovered process to the intact heart function and its therapeutic potential.
We want to see how much protein acetylation matters when operating alongside all the other processes in the heart and the body, Shroff said. If this process is shown to be significant under these conditions, it will be an exciting finding.
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| Contact: Morgan Kelly mekelly@pitt.edu 412-624-4356 University of Pittsburgh Source:Eurekalert |