Role of HDAC6 in regulating heart stiffness
The enzyme, histone deacetylase 6 (HDAC6), has been studied in the context of many diseases, including heart disease; recently discovered a new role for HDAC6 in the regulation of myofibrils, the contractile units of the heart.

Researchers found evidence that HDAC6 acts on titin, a massive myofibril protein that contributes to heart stiffness. HDAC6 appears to remove a chemical modification known as acetylation from titin. When HDAC6 is inhibited, titin causes the heart to become stiffer; when HDAC6 is activated, the heart becomes less stiff. In the future, once cardiologists determine which type of dysfunction a patient has, it might be possible to therapeutically adjust HDAC6 enzymatic activity or levels to help the heart to pump and relax at an optimal stiffness.

The data suggest that in some cases, if you inhibit this enzyme, the heart might get too stiff; research firmly support continued clinical development of HDAC6 inhibitors, since this class of compounds holds great promise for treating a variety of devastating diseases, including certain forms of heart failure.