Abstract
Neonatal jaundice is commonly seen in early postnatal days, and a considerable proportion of cases are caused by hemolysis. It has been found that hemolytic jaundice in neonates is often accompanied with myocardial injury, which may pose a threat to their health. However, the pathogenic mechanism remains unclear. This review focuses on the potential mechanisms of myocardial injury associated with hemolytic jaundice, particularly highlighting the role of carboxyhemoglobin (COHb) as a potential contributor. Emerging evidence suggests that elevated COHb levels may alter the oxygen dissociation curve, thereby exacerbating myocardial hypoxia and subsequent cellular damage, especially in neonates who are highly sensitive to hypoxia. The review aims to improve early prediction, detection, and intervention for hemolytic jaundice-associated myocardial injury, while providing novel therapeutic strategies and potential targets.