Contact: Jessica Studeny
Case Western Reserve University
Caption: In the top row are schematic illustrations of a heart. The left and right ventricles are shown in cross section. In the middle row are photographs of whole mouse hearts as shown in Figure 3 of the Cell paper. In the bottom row are still images from high-resolution heart ultrasounds from mice taken from Figure 3 of the paper. A cross section of the left ventricle is outlined in yellow. A normal heart is shown in the left column. After stress or injury (such as mechanical overload or bombardment with adrenaline), the heart becomes enlarged, develops thickened walls that are laden with scar tissue, and eventually fails to pump blood normally (middle column). However, if the stressed heart is treated with the BET bromodomain inhibitor JQ1 (right column), this disease process is arrested. JQ1 treated hearts do not develop massive enlargement, scar tissue, or compromised pumping function. In fact, mice treated with JQ1 had maintained healthy-appearing and vigorously contracting hearts despite continuous exposure to very high levels of stress. These findings form the rationale for developing BET bromodomain inhibitors, such as the prototype drug JQ1, into novel targeted therapies for heart disease. Reference: Anand, Brown and Lin, et al. Cell 2013.
Credit: Adapted from Anand, Brown and Lin, et al. Cell 2013.
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