YAP-mediated glycolysis promotes pulmonary arterial smooth muscle cell proliferation in pulmonary arterial hypertension.

ABSTRACT: Glycolytic shift is implicated in the pathogenesis of pulmonary arterial hypertension (PAH). 6-Phosphofructo-2-kinase/fructose-2,6-biphosphatase 3 (PFKFB3) has been identified as a key enzyme regulating glycolysis. However, the molecular mechanisms underlying PFKFB3 regulation and glycolysis reprogramming in PAH remain unclear. Here, primary cultured pulmonary arterial smooth muscle cells (PASMCs) and monocrotaline-induced PAH rats were used to investigate these unknown mechanisms. We found that PFKFB3 expression and PASMC glycolysis were significantly increased in high mobility group box 1 (HMGB1)-treated cells, accompanied by the dephosphorylation and nuclear translocation of Yes-associated protein (YAP) via Rho-associated protein kinase signaling. Activation of YAP then acted as a trans

SUBMITTER: Shi W 

PROVIDER: S-EPMC12664026 | biostudies-literature | 2025 Oct

REPOSITORIES: biostudies-literature