Pulmonary hypertension (PH) is a severe cardiovascular syndrome characterized by progressively elevated pulmonary arterial pressure and driven pathologically by sustained vasoconstriction and irreversible vascular remodeling. Growing evidence underscores the central role of calcium ion (Ca 2+ ) signaling networks in PH pathogenesis, which dynamically regulate vascular smooth muscle cell (VSMC) contraction, proliferation, metabolic reprogramming, and endothelial–mesenchymal transition. This review summarizes recent advances in three key areas: (1) the molecular mechanisms of Ca 2+ signaling dysregulation in PH, with emphasis on the causal relationship between disrupted calcium homeostasis and pathological vascular remodeling; (2) the multidimensional crosstalk among transmembrane calcium channels—including voltage‐dependent calcium channels (VDCCs), store‐operated calcium channels (SOCCs), receptor‐operated calcium channels (ROCCs), and mechanosensitive channels (MSCs)—and their dynamic roles in driving PH progression through vascular wall cell contraction, proliferation, immune‐inflammatory responses, and related pathways; and (3) calcium channel‐targeted therapeutic strategies, highlighting recent progress in the development of pharmacological agonists and inhibitors for the management of PH.
Wu et al. (Thu,) studied this question.