ArticleScientific reports2026
HMGB1 drives pulmonary arterial smooth muscle cell proliferation and migration via the MAP2K3/p38 pathway in pulmonary vascular remodeling.
Article in Scientific reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
Pulmonary vascular remodeling (PVR) is primarily driven by the aberrant proliferation and migration of vascular cells, with pulmonary artery smooth muscle cells (PASMCs) playing a central role. High mobility group protein B1 (HMGB1), a damage-associated molecular pattern (DAMP) molecule, is released via apoptosis, necrosis, or inflammatory cell activation and contributes to the pathological progression of various cardiopulmonary diseases. However, the mechanism by which HMGB1 regulates PASMCs to participate in PVR remains to be elucidated. PASMCs were stimulated with recombinant HMGB1. Proliferation of PASMCs was detected using CCK-8 and EdU assays, and migration of PASMCs was assessed by cell scratch and Transwell experiments. RNA-Seq was performed to profile transcriptomic changes in HMGB1-treated PASMCs, followed by bioinformatic analysis to identify DEGs and associated signaling pathways. Validation of DEGs was conducted using qRT-PCR and Western blotting. Monocrotaline (MCT) constructs a rat pulmonary vascular remodeling model to verify protein expression levels. HMGB1 treatment upregulated MAP2K3 expression and activated p38 phosphorylation in PASMCs, driving cell proliferation and migration. Silencing MAP2K3 or administering the p38 inhibitor SB203580 reversed the HMGB1-induced cellular functional changes and downregulated the expression of inflammatory cytokines (IL-1β, IL-6, TNF-α). HMGB1 also upregulated the Bcl-2/Bax ratio, inducing apoptosis resistance, while the inhibitors restored apoptotic balance. In a rat model of MCT-induced pulmonary vascular remodeling, MAP2K3 expression and p38 phosphorylation levels were significantly elevated, accompanied by pathological changes such as vascular wall thickening and increased muscularization. In addition, intervention with the HMGB1 inhibitor glycyrrhizin or SB203580 blocked MAP2K3/p38 activation, alleviated pulmonary vascular remodeling, inhibited cell proliferation, and restored apoptotic balance. This study elucidates that HMGB1 may drive PASMC proliferation and migration via the MAP2K3/p38 signaling axis, thereby contributing to pulmonary vascular remodeling. These findings provide new ideas for the treatment of pulmonary vascular remodeling diseases.
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.