ArticleScientific reports2026
aFGF rescues high glucose-induced senescent fibroblasts and improves diabetic wound healing by regulating SIRT1/STAT3 pathway.
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
12 authors.
Funding
Abstract
In the wound of diabetic patients, Fibroblasts are extensively senescent and dysfunctional, resulting in prolonged skin wound healing time. The aim of this study was to investigate the impact of aFGF on diabetic wound healing and the senescence of fibroblasts induced by high glucose, and to explore the underlying mechanisms. We injected aFGF locally into the back wound of (Streptozocin) STZ-induced diabetic rats, and subsequently assessed its therapeutic impact on wound healing in vivo by measuring the wound healing rate and the expression of aging markers. Next, we conducted a series of in vitro experiments utilizing HG-induced L929 fibroblasts to evaluate the effects of aFGF on their aging and modulation of oxidative stress. Finally, we evaluated the changes of SIRT1 expression levels and phosphorylation STAT3 (Y705) levels, and observed whether the therapeutic effect of aFGF on diabetic wounds is related to the regulation of this pathway. Local injection of aFGF into diabetic wounds accelerates wound closure and decreases senescence associated secretory phenotype (SASP) expression. In vitro, aFGF enhanced the anti-senescence and antioxidant capacity of HG-induced senescent fibroblasts. It was found that aFGF effectively rescued SIRT1 expression and inhibited STAT3 phosphorylation in senescent tissue of diabetic wound. Our findings suggested that aFGF ameliorates the dysfunction of senescent fibroblasts by modulating the SIRT1/STAT3 signaling axis, thereby accelerating diabetic wound healing. aFGF is a promising therapeutic candidate for the treatment of diabetic wounds.
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.