ReviewFrontiers in immunology2025
Macrophage-driven immunopathology in pulmonary arterial hypertension: from mechanisms to targeted therapies.
Review in Frontiers in immunology, 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.
- Transcriptomic Profiling Identifies Disease-Specific miRNA-mRNA Regulatory Networks in Systemic Sclerosis.Biomolecules · 2026Article
- Beyond the Vasculature: The Emerging Role of Systemic Metabolism and Immunometabolism in Pulmonary Arterial Hypertension.International journal of molecular sciences · 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
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pulmonary arterial hypertension (PAH) is a progressive vascular disorder characterized by obstructive vascular remodeling driven by the aberrant proliferation of endothelial cells, smooth muscle cells, and adventitial fibroblasts within the small pulmonary arteries. Emerging evidence highlights a pivotal role for macrophage polarization in PAH pathogenesis. In the pulmonary vasculature, macrophages drive local inflammation and fibrosis through M1/M2 polarization, while the inflammatory mediators they release can also alter the systemic immune environment and indirectly influence right ventricular remodeling through the "lung-heart immune axis." This phenotypic plasticity is tightly governed by hypoxia-induced signaling pathways, metabolic reprogramming, and epigenetic modifications. Elucidating these mechanisms has revealed macrophage polarization and immunometabolic regulation as promising therapeutic targets for PAH. Future investigations focusing on macrophage heterogeneity, single-cell transcriptomics, and precision immunomodulatory strategies are expected to accelerate the development of targeted therapies and improve clinical outcomes in PAH.
Indexed as
Identifiers
What Socratic holds
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.