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Article 2025 · 0 citations

The role of transforming growth factor beta-1 (TGF-<i>β</i>1) in the development of fibrosis in keratoconus

Yildirim, Mustafa

Abstract

BackgroundThe etiology of keratoconus, a disease characterized by deterioration in the extracellular matrix and thinning of the corneal stroma, has not yet been fully elucidated. Recent studies have drawn attention to the relationship between TGF-beta 1 (Transforming Growth Factor Beta-1) and keratoconus because of its essential role in extracellular matrix secretion. AimsThis study aimed to assess serum TGF-beta 1 levels in keratoconus patients and demonstrate its potential for estimating the severity of the disease. Materials and methodsThe study prospectively included 63 patients diagnosed with keratoconus, followed-up between October 2023 and May 2024, and 65 healthy individuals. Patients were divided into four groups according to the Amsler-Krumeich classification. Serum TGF-beta 1 levels were measured from venous blood samples taken from the patient and control groups using ELISA. ResultsIn the patient group, TGF-beta 1 levels were 357.13 pg/ml (165.43-793.91) and 233.71 pg/ml (117.95-583.72) in the control group. TGF-beta 1 levels in the patient group were significantly higher than in the control group (p = 0.001). When keratoconus was examined according to stage, it was determined that TGF-beta 1 levels increased as the severity of the disease increased (p < 0.05 for all groups). No statistical difference was found between the groups in terms of age and gender. ConclusionConsidering that TGF-beta 1 is effective in the formation of fibrosis, high TGF-beta 1 levels may play a role in the scar formation observed in the advanced stages of keratoconus patients.

Keywords
Fibrosis Keratoconus Transforming growth factor beta-1 TGF-BETA EXPRESSION GENES
WoS Categories
Medicine, General & Internal
Sustainable Development Goals
Citation
Journal
IRISH JOURNAL OF MEDICAL SCIENCE
Year
2025
Volume
194
Issue
5
Pages
1685-1689
ISSN
0021-1265
eISSN
1863-4362
DOI
10.1007/s11845-025-04029-9
WoS UID
WOS:001545937600001
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