Myocardial infarction treatment through hypoxic environment and Т3 inhibitors: А hypothesis from existing studies

Myocardial infarction is one of the leading causes of global mortality and is strongly associated with permanent damage and sudden cardiac death. The human heart loses its proliferative ability after birth as cardiomyocytes are compelled to differentiate into mature cells focusing on hypertrophy. Based on the review of existing studies, we hypothesised that the combination of hypoxia and 3, 3', 5-triiodo-L-thyronine (T 3 ) inhibitors could potentially be a more sustainable treatment method. We searched trusted scientific databases, such as PubMed, Directory of Open Access Journals (DOAJ), and Scopus, for relevant studies. T 3 is a physiological hormone that was found to promote cardiomyocyte differentiation and inhibit its proliferation. Studies implied that inhibiting T 3 during perinatal development could preserve the heart’s proliferative and regenerative capacities for a more extended period. Several animal experiments and human studies have found that inducing a hypoxic environment could revert cardiomyocytes to their endogenous proliferative state. However, long periods of hypoxia were not sustainable due to its deleterious effects on the human body. We suggested that administering T 3 inhibitors after the cardiomyocytes have been reverted under hypoxic conditions could enable patients to leave the hypoxic environment while preventing physiological maturation by T 3 , thus preserving the heart’s regenerative capacity.