ArticleScientific reports2025
Unphosphorylated STAT1 binds to the BST2 transcription promoter, promoting increased AKBA anchoring on HPMECs to alleviate ARDS.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Emerging Oncogenic and Immunoregulatory Roles of BST2 in Human Cancers.Biomedicines · 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
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although the drug therapeutic targets of acute respiratory distress syndrome (ARDS) are still unclear and no specific drugs for ARDS treatment have been found, some breakthroughs have been gradually made in the biological target pathways such as endothelial injury. The Traditional Chinese Medicine Systems Pharmacology (TCMSP) database suggests that Acetyl-11-keto-β-boswellic acid (AKBA), a processed product of boswellic acid, may be an effective intervention for ARDS. After preliminary in vitro and in vivo verification of the protective role of AKBA on ARDS, in order to explore the mechanism of AKBA in ARDS, we used transcriptomic and proteomic methods to explore its main targets, and used molecular docking and cell thermal shift assay (CETSA) to further reveal the potential value of bone marrow stromal cell antigen 2 (BST2) as a target. We subsequently examined the effect of AKBA targeting BST2 on tubule formation, cell proliferation (Colony formation and EdU assay), migration (transwell and scratch assays), apoptosis and autophagy levels both in vitro and in vivo, and protein changes (analyzed by Western blotting analysis). Our results show that the unphosphorylated signal transducers and transcription activation factors (U-STAT1) bins to the BST2 transcription promoter to encourage more AKBA anchoring the human pulmonary microvascular endothelial cells (HPMECs), thus inhibiting apoptosis and autophagy, promoting migration and tube formation, and restraining the cecal ligation and puncture (CLP) induced lung tissue damage in mice. In conclusion, AKBA treatment may be a potential strategy in the intervention of ARDS. Alternatively, BST2 may contribute to the anchoring of AKBA to HPMECs, and STAT1 as a transcription factor promoting BST2 expression may bind to its promoter.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.