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Myocardial ischemia-reperfusion (IR) injury is associated with structural alterations involving both the necrotic and the non-necrotic myocardium. These changes are referred to as myocardial remodeling. In addition to the loss of critical cardiomyocyte mass through cell death, there are further structural alterations associated with scarring, as well as changes in a family of endogenous enzymes, the matrix metalloproteases (MMP), which cause loss of myocardial extracellular matrix (ECM) [Janssens S, Lijnen HR. What has been learned about cardiovascular effects of matrix metalloproteinases from mouse models. Cardiovasc Res 2006;69:585-594., Wainwright CL. Matrix metalloproteinases, oxidative stress and the acute response to acute myocardial ischaemia and reperfusion. Curr Opin Pharmacol 2004;4:132-138.]. The chemokine TGFbeta1, which has wide-ranging effects upon cells and tissues, is showing promise as a useful drug/agent for the limitation of IR injury. Coupled with the identification of TGFbeta1 as a therapeutic agent for IR treatment are investigations into its mode of delivery to the patient. Gene therapy utilizing delivery by viral vectors is just one of many possible ways to deliver TGFbeta1 for IR treatment. In this review we discuss the mechanisms of action of TGFbeta1 and how it might be delivered successfully to patients under risk of or who are actively undergoing acute IR injury.

Mechanism of action and delivery possibilities for TGFβ1 in the treatment of myocardial ischemia