ArticleJournal of translational medicine2025
PHPT1 acts as an inhibitor in high-altitude pulmonary hypertension via negative TRPV5 signaling regulation.
Article in Journal of translational medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundLow barometric pressure hypoxia at high altitudes triggers vascular remodeling, resulting in high-altitude pulmonary hypertension (HAPH). The key step is the transformation of pulmonary artery smooth muscle cells (PASMCs) from a contractile to synthetic phenotype. Protein kinases and phosphatases contribute to phenotype transformation by altering phosphorylated protein expression.
objectivesIn this study, we aimed to investigate the role of phosphohistidine phosphatase 1 (PHPT1) in PASMC transformation and its regulatory pathway in HAPH.
methodsAn HAPH model was constructed in wild-type, PHPT1
resultsPHPT1 protein expression was downregulated in HAPH, and its knockdown impaired cardiopulmonary functions, including elevated mean pulmonary artery pressure (mPAP), right ventricular systolic pressure (RVSP), and increased right ventricular thickness, and enhanced PASMC proliferation and migration. PHPT1 directly interacted with TRPV5 phosphorylation sites, whereas Asp30Ala/Arg157Ala functioned to prevent this interaction. PHPT1 overexpression protected against cardiopulmonary damage, reducing mPAP, RVSP, the D/W ratio, and MWT%. Additionally, PHPT1 overexpression mitigated PASMC proliferation and migration, resulting in restored TRPV5, p-Akt, p-SMAD2/3, and p-TGF-β expression under hypoxic conditions.
conclusionsThese findings underscore that PHPT1 inhibits PASMC proliferation and migration through TRPV5 signaling, thereby reducing mPAP and improving right ventricular function in HAPH. Therefore, PHPT1 targeting could potentially contribute to the development of novel therapeutic approaches for treating HAPH.
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