Application of TIMP2 leads to enhanced synaptic plasticity and improved cognitive function in mice;  TIMP2 deficiency inhibits cardiac remodeling processes after myocardial infarction in mice via inhibition of membrane type 1 matrix metalloproteinase;  involved in homing mechanisms of human mesenchymal stem cells;  elevated plasma levels of TIMP1, TIMP2 and TIMP4 have been associated with higher risk for major adverse cardiac events after acute myocardial injury in humans. Here, TIMP1 is linked to myocardial infarction.