ReviewAmerican heart journal plus : cardiology research and practice2025
NF-κB and pulmonary hypertension: Advances in mechanistic research and therapeutic applications.
Review in American heart journal plus : cardiology research and practice, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- Vitamin D Attenuates Inflammation and Mitochondrial Dysfunction in Experimental Models Relevant to Connective Tissue Disease-Associated Pulmonary Arterial Hypertension.Food science & nutrition · 2026Article
- NF-κB signaling as a critical inflammatory node in pulmonary arterial hypertension: from vascular remodeling to right heart failure.Frontiers in immunology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.