Finally, as PDNF binding to TrkA on fibroblasts releases NGF (Fig. 6) which, in turn, protects cardiomyocytes against oxidative stress (Fig. 8B) and perhaps other insults [10], and, as intravenous administration of sPDNF boosts cardiac NGF (Fig. 7), our results offer a possible novel translational medicine opportunity for cardiomyopathies where NGF gene therapy has proven to be valuable in myocardial infarction [12] and diabetes [52]. The gene discussed is NGF; the disease is myocardial infarction.