HSPB1 and myocardial infarction: In a rat MI model and a primary cardiomyocyte hypoxia model (117), cardiomyocytes overexpressing ANT1 had enhanced HSP27 expression and secretion under hypoxic conditions; the secreted HSP27 induced the expression of HSP27 and ANT1 by stimulating TLR4-dependent AKT activation.