Fig. 7

Putative roles of YULINK in PDGF- or MCT-induced PAH pathological aberrations. During PAH-related pathogenesis induced by PDGF or MCT, an increase in YULINK expression occurs. YULINK coordinates with GLUT1 to facilitate glucose uptake, accompanied by an upregulation of HK-2, promoting enhanced glycolysis in PASMCs. This increased YULINK expression also contributes to uncontrolled cell migration and proliferation through the PDGFR-PI3K-AKT signaling pathways. While numerous reports have highlighted the role of this pathway in glucose metabolism and the Warburg effect, whether the triggered PI3K-AKT signaling regulates PAH-related processes requires further investigation. Suppression of YULINK through gene knockdown or the use of an inhibitor LY294002 to suppress PI3K activation has the potential to reverse these pathological abnormalities associated with PAH. In this graph, the black arrows represent the signaling transduction pathways, and the red arrows denote the enhancements in response to PAH pathogenesis. The dotted lines summarize findings from other published literature, not experiments conducted in this manuscript