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Taking TIMP3 to heart

A U.S. team has found a way to harness the cardioprotective activity of tissue inhibitor of metalloproteinases 3 while avoiding its off-target effects by embedding it in a hydrogel for direct injection into the heart.1 Although preclinical data show that local delivery of the molecule could help prevent heart failure after myocardial infarction in patients with ventricular dilation, it may have a detrimental effect in other patients, making patient selection critical.

After myocardial infarction (MI), left ventricular wall damage is partly caused by overactive matrix metalloproteinase (MMP) enzymes that break down extracellular matrix in the ischemic tissue.

Under normal conditions, tissue inhibitors of metalloproteinases (TIMPs) control MMP activity and help regulate the breakdown of matrix proteins. After MI, however, there is an increase in MMP plasma levels without a matching change in levels of TIMPs, creating an imbalance in

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