Targeted knockout of PFKFB3 leads to a significant reduction in EC glycolysis and effectively inhibits the NF-κB and HIF-1α signalling-mediated endothelial inflammatory response, thereby impeding the onset and progression of pulmonary hypertension, sepsis, and acute lung injury in murine models [180, 181]. Here, HIF1A is linked to pulmonary arterial hypertension.