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Background <p>Pulmonary hypertension (PH) is a complicated cardiovascular disorder marked by elevated pulmonary arterial pressure and vascular remodeling. The molecular interplay between Ryanodine Receptor 2 (RyR2) and FK506-binding protein 12.6 (FKBP12.6) emphasizes that their dissociation under hypoxic conditions results in intracellular calcium(Ca²⁺) dysregulation in pulmonary artery smooth muscle cells (PASMCs).</p> Objective <p>This review article highlights important discoveries about how mitochondrial ROS, particularly those mediated by the Rieske iron-sulfur protein (RISP), trigger RyR2 activation and the sub sequent release of Ca2+. Furthermore, it covers a process that establishes a connection between sarcoplasmic reticulum calcium signaling, which promotes vasoconstriction and vascular remodeling, and mitochondrial dysfunction.</p> Conclusion <p>The pathways involved inRyR2/FKBP12.6 destabilization lead to progression in PH. Moreover, targeting these pathways has been reported to be beneficial in PH management.</p> Graphical Abstract <p></p>

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Crosstalk between Ryanodine Receptor 2 Dysfunction and FK506-Binding Proteins in Pulmonary Hypertension

  • 期刊论文

  • 发表日期：

    2025年12月13日

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  • Janavie Patel,
  • Gaurav Doshi

摘要

Background

Pulmonary hypertension (PH) is a complicated cardiovascular disorder marked by elevated pulmonary arterial pressure and vascular remodeling. The molecular interplay between Ryanodine Receptor 2 (RyR2) and FK506-binding protein 12.6 (FKBP12.6) emphasizes that their dissociation under hypoxic conditions results in intracellular calcium(Ca²⁺) dysregulation in pulmonary artery smooth muscle cells (PASMCs).

Objective

This review article highlights important discoveries about how mitochondrial ROS, particularly those mediated by the Rieske iron-sulfur protein (RISP), trigger RyR2 activation and the sub sequent release of Ca2+. Furthermore, it covers a process that establishes a connection between sarcoplasmic reticulum calcium signaling, which promotes vasoconstriction and vascular remodeling, and mitochondrial dysfunction.

Conclusion

The pathways involved inRyR2/FKBP12.6 destabilization lead to progression in PH. Moreover, targeting these pathways has been reported to be beneficial in PH management.

Graphical Abstract