Why the study?
Pulmonary hypertension has a complex etiology, high mortality rate, and no cure, prompting the exploration of novel therapeutic strategies such as targeting JP2.
Targeting Junctophilin-2 (JP2) may offer a novel therapeutic approach for pulmonary hypertension by modulating vascular smooth muscle contraction and remodeling.
JP2 may represent a PH therapeutic target; leaves open clinical translation from preclinical findings.
Pulmonary hypertension (PH) is a disease with a complex etiology and high mortality rate. Abnormal pulmonary vasoconstriction and pulmonary vascular remodeling lead to an increase in mean pulmonary arterial blood pressure for which, and there is currently no cure. Junctophilin-2 (JP2) is beneficial for the assembly of junctional membrane complexes, the structural basis for excitation-contraction coupling that tethers the plasma membrane to the sarcoplasmic reticulum/endoplasmic reticulum and is involved in maintaining intracellular calcium concentration homeostasis and normal muscle contraction function. Recent studies have shown that JP2 maintains normal contraction and relaxation of vascular smooth muscle. In some experimental studies of drug treatments for PH, JP2 expression was increased, which improved pulmonary vascular remodeling and right ventricular function. Based on JP2 research to date, this paper summarizes the current understanding of JP2 protein structure, function, and related heart diseases and mechanisms and analyzes the feasibility and possible therapeutic strategies for targeting JP2 in PH.
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Tan et al. (2021) studied this question.
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