Fig. 1 |. Response and therapeutic approaches to myocardial injury.

a | Response tomyocardial injury differs between developmental stages in mice. Neonatal mice (aged <1 week) are capable of regenerating the heart, with functional recovery after injury.This regenerative capacity is lost postnatally after the first week. b,c | In adult mice and humans, the default response to myocardial injury is fibrosis, where the infarct necrotic tissue is replaced with a fibrotic scar, causing loss of cardiac contractility. The damaged adult heart enters a negative loop of cardiac remodelling that progresses to heart failure. In humans, the current goal of clinical therapies is either to salvage the ischaemic myocardium by early revascularization (light grey box) or to prevent cardiac remodelling with drug therapy and electromechanical support (dark grey box). Accumulating evidence in preclinical studies demonstrates promising outcomes with therapeutic approaches aimed at heart regeneration (green box), although these new approaches have clinical translational problems. The dashed line indicates potential clinical therapeutic approaches. ACE, angiotensin- converting enzyme; ARNI, angiotensin receptor–neprilysin inhibitor ; CRT, cardiac resynchronization therapy; LVAD, left ventricular assist device; MR, mineralocorticoid receptor ; PCI, percutaneous coronary intervention.