ApoE and adiponectin are also important downstream effectorsof PPARγ, both of which inhibit smooth muscle cell proliferation by convergingon the PDGFR-β pathway.84 Reduced ApoE expression has been observed in the lungs of IPAH patients,suggesting that the BMPR2/PPARγ/ApoE axis may be a key mediator of theassociation between insulin resistance and PAH.85 This evidence concerns the gene APOE and pulmonary arterial hypertension.