Evidence mapPaperPMID 42397137Full record

ArticleInternational wound journal2026

Immunoinflammatory Profile of FGF-18, IL-35 and Glutamic Acid Decarboxylase in Patients With Diabetic Foot Ulcers.

Hemin Mohamad Hussein, Ahmed Alkhuzai, Shukur Wasman Smail, Taha Othman Mahwi, Jonas Bystrom, Christer Janson, Kawa Amin

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Article in International wound 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.

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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.

2 · The registry

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4 · The record

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5 · Who and what money

Authors and funding

7 authors.

Hemin Mohamad HusseinDepartment of Biology, College of Science, University of Sulaimani, Sulaymaniyah, Iraq.
Ahmed AlkhuzaiDepartment of Clinical Sciences, College of Medicine, University of Sulaimani, Sulaymaniyah, Iraq.
Shukur Wasman SmailCollege of Pharmacy, Cihan University-Erbil, Erbil, Kurdistan Region, Iraq.ORCID https://orcid.org/0000-0001-8188-2540
Taha Othman MahwiDepartment of Clinical Sciences, College of Medicine, University of Sulaimani, Sulaymaniyah, Iraq.
Jonas BystromCentre for Translational Medicine and Therapeutics, William Harvey Research Institute, Queen Mary University of London, London, UK.
Christer JansonDepartment of Medical Science, Respiratory Allergy and Sleep Research, Uppsala University, Uppsala, Sweden.
Kawa AminDepartment of Medical Science, Respiratory Allergy and Sleep Research, Uppsala University, Uppsala, Sweden.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diabetic foot ulcer (DFU) is a serious problem that may cause amputation of the lower extremities in patients with diabetes. The present research aimed to assess the localised tissue expression and potential immunoinflammatory crosstalk among fibroblast growth factor-18 (FGF-18), glutamic acid decarboxylase (GAD) and interleukin-35 (IL-35) in DFU compared to non-diabetic controls (NDCs), while also examining the systemic serum levels of FGF-18 and IL-35. Venous blood was collected from 80 patients with DFU and 100 NDC, and the concentrations of serum IL-35, FGF-18 and blood haemoglobin A1c (HbA1c) were analysed. Aseptically collected biopsy samples were obtained from FUs of 30 type 2 diabetes (T2D) patients and from accidental foot wounds of 30 NDC. Biopsies were preserved in formalin (10%) until paraffin blocks were prepared. The immunohistochemical methodology used antibodies specifically to identify tissue FGF-18, GAD and IL-35 in the soft tissue specimens. The tissue expression of FGF-18, IL-35 and GAD was significantly higher in DFU compared to NDC (p ≤ 0.0001), suggesting a strong localised immunoinflammatory role, whereas serum levels of FGF-18 and IL-35 remained statistically unchanged. Furthermore, significant positive correlations observed between tissue IL-35 and FGF-18 (r = 0.67, p ≤ 0.05) and between tissue IL-35 and GAD (r = 0.60, p ≤ 0.05) indicate robust immunoinflammatory crosstalk. The marked and correlated elevation of FGF-18, IL-35 and GAD specifically within DFU tissue, without changes in serum levels of FGF-18 and IL-35, establishes a robust, compartmentalised immunoinflammatory axis that drives chronic pathology and presents novel targets for localised therapeutic intervention.

Indexed as

Diabetes Mellitus, Type 2Diabetic FootFibroblast Growth FactorsGlutamate DecarboxylaseInterleukinsAdultAgedFemaleHumansMaleMiddle AgedFibroblast Growth FactorsGlutamate Decarboxylaseinterleukin-35, humanInterleukinsdiabetic foot ulcerfibroblast growth factor‐18glutamic acid decarboxylaseIL‐35inflammationtype 2 diabetes

Identifiers

PMID42397137
PMCPMC13330589

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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.