CCN5 and myocardial infarction: The study discloses the novel findings that CCN5 is transcriptionally induced by catecholamines acting through β2-adrenergic receptors on endothelial cells and cardiac fibroblasts and repressed by TNF-α through NF-κB suppressor elements, i.e. factors that are elevated following myocardial infarction and during ischemic heart failure.