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Updated: Sep 21, 2025

Ex Vivo Corneal Organ Culture Model for Wound Healing Studies
Published on: February 15, 2019
Galectin 1-A Key Player between Tissue Repair and Fibrosis
Anca Hermenean1,2, Daniela Oatis1, Hildegard Herman2
1Faculty of Medicine, Vasile Goldis Western University of Arad, 310414 Arad, Romania.
Galectin-1 (Gal-1) influences wound healing phases and can cause keloid scarring when overexpressed. Modulating Gal-1 offers therapeutic potential for wound healing and treating various fibrotic diseases, including diabetic retinopathy.
Area of Science:
- Biochemistry
- Molecular Biology
- Immunology
Background:
- Galectins are carbohydrate-binding proteins, with Galectin-1 (Gal-1) being a key member.
- Gal-1 is expressed in various tissues and plays roles in both normal physiological processes and pathological conditions.
Purpose of the Study:
- To review the dual role of Galectin-1 in wound healing, distinguishing between beneficial modulation and detrimental overexpression.
- To explore the involvement of Galectin-1 in the pathogenesis of fibrotic diseases across multiple organs.
Main Methods:
- Literature review focusing on studies investigating Gal-1's impact on wound healing phases (inflammation, proliferation, repair, re-epithelialization).
- Analysis of research on Gal-1's role in fibrotic conditions such as proliferative diabetic retinopathy, liver, renal, pancreatic, and pulmonary fibrosis.
- Examination of molecular pathways, including PI3K/Akt, implicated in Gal-1's effects.
Main Results:
- Gal-1 positively modulates distinct phases of wound healing.
- Persistent overexpression of Gal-1 promotes angiogenesis and extracellular matrix production via PI3K/Akt activation, leading to keloid formation.
- Gal-1 is implicated in the pathogenesis of diverse fibrotic diseases.
Conclusions:
- Targeted modulation of Gal-1 presents a therapeutic strategy for optimizing wound healing and preventing keloid scarring.
- Gal-1 shows promise as a diagnostic/prognostic biomarker for tissue fibrosis.
- Gal-1 represents a potential molecular target for novel antifibrotic therapies in chronic diseases.
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