The role and mechanism of heat shock proteins in the development of pulmonary arterial hypertension.

Pulmonary arterial hypertension (PAH) is a progressive pulmonary vascular disease characterized by increased pulmonary vascular resistance, right ventricular overload and premature death. Current therapies improve symptoms and hemodynamics but do not adequately reverse pulmonary vascular remodeling. Heat shock proteins (HSPs), key regulators of proteostasis and stress adaptation, are increasingly implicated in PAH pathogenesis. Among them, Hsp70, Hsp90 and Hsp110 have attracted particular interest because of their distinct roles in chaperone networks and vascular remodeling. This review summarizes the structural and functional features of these HSPs, their roles in PAH-associated remodeling and the therapeutic potential and challenges of HSP-targeted strategies.