Therefore, we hypothesize that: on one hand, under conditions of persistent ferroptosis activation, the expression of SLC7A11 may be negatively regulated by ATF4, thereby antagonizing the transcriptional activation effect of Nrf2 on it; on the other hand, with the increase in concentration, PAH-induced ferroptosis gradually enhances the inhibition of SLC7A11 protein expression, leading to a decrease in intracellular SLC7A11. Here, SLC7A11 is linked to pulmonary arterial hypertension.