ACSL4 and persistent truncus arteriosus: Through lipidomics and RNA sequencing, Bi et al. observed a marked increase in ACSL4 expression in a heart failure model induced by TAC in mice, and ACSL4 overexpression in cardiomyocytes exacerbates the cardiac dysfunction triggered by pressure overload through ferroptosis.481 Notably, ACSL4-driven ferroptosis has been found to activate the pyroptosis pathway, leading to elevated levels of IL-1β.481 This suggests that ACSL4 initiates a cascade that links ferroptosis to pyroptosis, thereby promoting cardiac hypertrophy and responding to the hemodynamic stress induced by aortic constriction.