ABSTRACT
Clinical trials employing bone marrow-derived stem cells for treatment of myocardial infarction (MI) have shown short-term mechanical benefit.1,2 Whether this initial improvement is translated into long-term gain remains uncertain.3
These clinical studies were preceded by those in animal models demonstrating that stem cells delivered post-MI improve angiogenesis, myocardial wall movement, and possibly even myocyte content. However, the physiological mechanisms underlying these stem cell-induced improvements are poorly understood. It is not even certain whether the functional improvement derived from the delivered stem cells is mediated through improved active contraction or via changes in passive mechanical properties.4 In an attempt to understand the basis of any favorable effects of stem cells, as well as to enhance their efficacy, it seems natural to genetically engineer stem cells to optimize the expression of those factors thought most likely to be beneficial. Alternatively, stem cells could be engineered for enhanced survival so that their favorable actions would be prolonged.5
