Moreover, lack of ClC-3 promoted eNOS-Hsp90-Akt complex formation and eNOS disassociation from caveolin-1, and upregulation the phosphorylation of Akt.<h4>Discussion</h4>Our findings suggest that ClC-3 may serve as an important target for hypertension-related endothelial dysfunction, potentially providing new strategies and interventions for the treatment of hypertension and its complications. The gene discussed is CAV1; the disease is endothelial dysfunction.