Why the study?
The involvement of NF-κB signaling in pulmonary hypertension pathogenesis has attracted growing interest as evidence indicates it contributes to pulmonary vascular remodeling and right ventricular dysfunction.
NF-κB signaling plays a critical role in the pathogenesis of pulmonary hypertension, highlighting its potential as a therapeutic target.
Pulmonary hypertension (PH) is a severe cardiovascular disorder characterized by pulmonary arterial smooth muscle cells (PASMCs) proliferation and vascular remodeling. The nuclear factor-kappa B (NF-κB) family of transcription factors serves as a central mediator of inflammatory responses and plays a critical role in both innate and adaptive immunity. In recent years, the involvement of NF-κB signaling in PH pathogenesis has attracted growing interest. Accumulating evidence indicates that NF-κB contributes to pulmonary vascular remodeling and right ventricular (RV) dysfunction by modulating inflammatory processes, cell proliferation, and apoptosis. This review systematically summarizes the molecular mechanisms by which NF-κB contributes to PH, emphasizing its cell-specific roles in PASMCs and pulmonary arterial endothelial cells (PAECs), and evaluates the therapeutic potential of NF-κB as a target in PH.
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Si. et al. (2025) studied this question.
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