Galectins are ten family members of
carbohydrate-
binding proteins with a high affinity for β
galactose-containing
oligosaccharides.
Galectin-1 (Gal-1) is the first
protein discovered in the family, expressed in many sites under normal and pathological conditions. In the first part of the review article, we described recent advances in the
Gal-1 modulatory role on wound healing, by focusing on the different phases triggered by
Gal-1, such as
inflammation, proliferation, tissue repair and re-epithelialization. On the contrary,
Gal-1 persistent over-expression enhances angiogenesis and extracellular matrix (ECM) production via PI3K/Akt pathway activation and leads to
keloid tissue. Therefore, the targeted
Gal-1 modulation should be considered a method of choice to treat wound healing and avoid
keloid formation. In the second part of the review article, we discuss studies clarifying the role of
Gal-1 in the pathogenesis of proliferative
diabetic retinopathy, liver, renal, pancreatic and
pulmonary fibrosis. This evidence suggests that
Gal-1 may become a
biomarker for the diagnosis and prognosis of tissue
fibrosis and a promising molecular target for the development of new and original therapeutic tools to treat
fibrosis in different
chronic diseases.