ArticleMolecular biology reports2026
Astragalus polysaccharide accelerates wound healing by targeting the miR-92a/FGF2 axis in dermal fibroblasts.
Article in Molecular biology 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
objectiveWound healing requires fibroblast activation, including proliferation, migration, and extracellular matrix (ECM) remodeling. Astragalus polysaccharides (APs), derived from Astragalus membranaceus, have been reported to promote tissue repair, but the underlying mechanisms remain unclear. This study examined whether APs facilitate wound healing through the miR-92a/FGF2 axis.
methodsHuman foreskin fibroblasts (HFF-1) were incubated with APs, and proliferation, migration, FGF2, and miR-92a expression were evaluated. Functional assays involved miR-92a overexpression or inhibition. A full-thickness skin defect rat model was utilized to assess wound closure and molecular changes following AP treatment with or without miR-92a agomir.
resultsAPs enhanced fibroblast proliferation and migration, increased FGF2 expression, and suppressed miR-92a levels. miR-92a directly targeted FGF2, thereby inhibiting fibroblast activity. Overexpression of miR-92a weakened the pro-healing effects of APs, whereas inhibition restored them. In rats, APs accelerated wound closure and elevated FGF2 expression, while miR-92a agomir impaired repair and reduced FGF2 expression.
conclusionAPs promote cutaneous wound repair by modulating the miR-92a/FGF2 axis, with miR-92a acting as a negative regulator. Targeting this pathway may strengthen the therapeutic potential of APs in skin regeneration.
Indexed as
Identifiers
42068430What 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.