Integrated Bioinformatics Analysis and In Vitro Evidence Support HSP90AA1 as a Candidate Target of Camellia petelotii (Merr.) Sealy in Pulmonary Arterial Hypertension

in fibroblasts and endothelial cells. Molecular docking and molecular dynamics simulations supported stable binding of luteolin to HSP90AA1. In vitro, CP extract inhibited hypoxia-induced hyperproliferation of RPASMCs and reduced HSP90AA1 protein expression. HSP90AA1 may represent a candidate molecular mediator of CP in PAH, and CP inhibited hypoxia-induced RPASMC proliferation in association with downregulation of HSP90AA1.