ArticleBalkan medical journal2026
Overexpression of Soluble Fibrinogen-like Protein 2 in MSCs Ameliorates Renal Ischemia-Reperfusion Injury in Mice by Modulating Neutrophils.
Article in Balkan medical journal, 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
No grant is acknowledged in the PubMed record.
Abstract
Background: Renal ischemia-reperfusion (I/R) injury is a major cause of graft dysfunction and failure, driving inflammation and tissue damage. Mesenchymal stem cells (MSCs) possess therapeutic potential due to their immunomodulatory properties. Notably, neutrophils express the inhibitory receptor CD32b, which is a specific target of the immunosuppressive molecule soluble fibrinogen-like protein 2 (sFgl2). Aims: To investigate the therapeutic efficacy and underlying mechanisms of genetically engineered MSCs expressing sFgl2 (sFgl2-MSCs) in treating renal I/R injury, with a focus on neutrophil regulation. Study Design: An Methods: Following imaging to localize MSCs, mice were randomly allocated into four treatment groups. Treatments were administered according to group assignments. Renal function was assessed using serum creatinine and blood urea nitrogen levels, while systemic inflammation was evaluated by measuring serum interleukin-1 beta (IL-1β), IL-6, tumor necrosis factor-alpha (TNF-α), and IL-10 via enzyme-linked immunosorbent assay (ELISA). Neutrophil proportions in the blood and kidney were analyzed by flow cytometry. At 24 h, surface expression of CD95 and CD206 was assessed; CD206 was used to define neutrophils with N2-like (CD206 Results: While unmodified MSCs exhibited a moderate therapeutic effect, sFgl2-MSCs treatment was significantly more effective. sFgl2-MSCs markedly improved renal function, reduced histopathological damage (e.g., tubular necrosis), and modulated systemic cytokine levels by decreasing pro-inflammatory (IL-1β, IL-6, TNF-α) and increasing anti-inflammatory (IL-10) cytokines. Crucially, sFgl2-MSCs regulated neutrophil responses in the kidney: they increased the proportion of N2-like neutrophils and decreased N1-like neutrophils, concurrently reducing NET-related markers, as evidenced by decreased CitH3 and cf-DNA. Mechanistically, sFgl2-MSCs enhanced neutrophil immunoregulatory function via the TGFβ-Smad2/3 signaling pathway. Conclusion: Genetically modified sFgl2-MSCs alleviate renal I/R injury. This protective effect is associated with engagement of neutrophil CD32b receptors, activation of the TGFβ-Smad2/3 pathway, promotion of a protective N2-like neutrophil phenotype, and suppression of N1-like and NET-related markers.
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.