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Treatment for Pulmonary Arterial Hypertension: Receptor Tyrosine Kinase Inhibitors and Calcium Channel Blockers01:26

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Imaging Ca2+ Signals in Small Pulmonary Veins at Physiological Intraluminal Pressures
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[Enhanced Ca2+-sensing receptor function in pulmonary hypertension].

Aya Yamamura1, Hisao Yamamura, Jason X-J Yuan

  • 1Kinjo Gakuin University School of Pharmacy.

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Summary

The extracellular calcium-sensing receptor (CaSR) is upregulated in pulmonary arterial hypertension (PAH), driving increased calcium signaling and smooth muscle cell proliferation. Blocking CaSR shows promise for treating this rare disease.

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Area of Science:

  • Cardiovascular Research
  • Cell Biology
  • Rare Diseases

Context:

  • Pulmonary arterial hypertension (PAH) is a progressive disease with a 5-year survival rate of approximately 50%.
  • Pathogenic mechanisms in PAH, including pulmonary vascular remodeling and vasoconstriction, are not fully understood.
  • Increased cytosolic calcium in pulmonary arterial smooth muscle cells (PASMCs) contributes to vasoconstriction and proliferation.

Purpose:

  • To investigate the role of the extracellular calcium-sensing receptor (CaSR) in idiopathic pulmonary arterial hypertension (IPAH).
  • To identify novel therapeutic targets for PAH by examining CaSR's contribution to disease pathogenesis.

Summary:

  • The extracellular calcium-sensing receptor (CaSR) is upregulated in PASMCs from IPAH patients.
  • Upregulated CaSR enhances calcium signaling and promotes PASMC proliferation, key events in PAH.
  • Blocking CaSR with an antagonist (NPS2143) ameliorated pulmonary hypertension in animal models.

Impact:

  • Identifies a novel pathogenic mechanism in IPAH involving CaSR.
  • Suggests CaSR as a potential therapeutic target for developing new PAH treatments.
  • Highlights the importance of calcium signaling pathways in the progression of pulmonary hypertension.