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Cardiac fibroblasts are resistant to several pro-apoptotic factors that prevail in the diseased myocardium. Resistance to death signals may, in the short-term, enable these cells to play a central role in tissue repair following myocyte loss but, in the long-term, facilitate their persistence in the infarct scar, resulting in disproportionate stromal growth and pump dysfunction. Surprisingly, the molecular basis of apoptosis resistance in cardiac fibroblasts remains unclear. We explored the recruitment of anti-apoptotic mechanisms in cardiac fibroblasts subjected to oxidative stress, a major component of ischemia–reperfusion injury and heart failure. Cardiac fibroblasts exposed to H₂O₂ expressed enhanced levels of anti-apoptotic cIAP-2 mRNA and protein, revealed by real time PCR and western blot analysis, respectively. Pulmonary fibroblasts did not express cIAP-2 and were more susceptible than cardiac fibroblasts to H₂O₂ …