ArticleBurns & trauma2025
MiR-23b-3p ameliorates sepsis-induced acute lung injury by inhibiting SMAD3-mediated endothelial-mesenchymal transition.
Article in Burns & trauma, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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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.
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Who cites it
3 citing papers in PubMed.
- A Computational Trial of Dermal Mechanotransduction in GLP-1 Receptor Agonist-Associated Premature Facial Ageing.Aesthetic plastic surgery · 2026Trial
- Review
- GLUT1 and GLUT3 in brain glucose metabolism: mechanisms, regulation, and implications for metabolic disorders.Metabolic brain disease · 2025Review
Corrections and comments
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Authors and funding
14 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Sepsis-associated acute lung injury (ALI) is driven by endothelial barrier dysfunction and endothelial-mesenchymal transition (EndoMT), mediated by TGF-β1/SMAD3 signaling. Despite the therapeutic potential of SMAD3, current inhibitors face limitations. As endogenous small molecules that are closely related to physiological regulatory processes, microRNAs (miRNAs) have more potential research value for regulating SMAD3. Therefore, this study aimed to investigate the protective effect and molecular mechanism of a key miRNA targeting SMAD3 in sepsis-ALI. Methods: Screening multiple databases revealed that Results: In LPS-stimulated HUVECs, Conclusion:
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Registered trials
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