In a study, CMs-specific deletion of PARP1 in Su/Hx-PAH mice and pharmacologic inhibition of PARP1 with olaparib or enforced PKM2 tetramerization with TEPP-46 in Prealbumin (PAB)-induced rats improved RV function, reduced fibrosis, inflammation, oxidative stress, and maladaptive remodeling by reversing glycolytic shifts and modulating metabolic and inflammatory pathways.343 Thus, targeting this axis therapeutically could restore metabolic balance and mitigate vascular remodeling in PAH. This evidence concerns the gene PARP1 and pulmonary arterial hypertension.