JUN and pulmonary arterial hypertension: Ma et al. demonstrated through in vitro experiments that epoxyeicosatrienoic acids, activates the c-Jun pathway by stimulating JNK and facilitating its translocation to the nucleus.165 This process leads to the upregulation of cell cycle-related proteins, promoting the transition from the G0/G1 phase to the S phase, while also inhibiting Caspase-3 activity, consequently, playing a pro-proliferative and anti-apoptotic role.165 However, in PAH mice that over-express IL-6, JNK was inhibited as a pro-apoptotic factor, indicating that JNK has a dual role in regulating apoptosis in PAH.154