Galectin-3 plays an important role in endometriosis development and is a target to endometriosis treatment

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Galectin-3 deficiency and Gal-3 carbohydrate recognition domain treatment reduced endometriotic lesion size, vascularization, and macrophage infiltration in mice.

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Abstract

This study aimed to analyze galectin-3 importance in endometriotic lesions development and the effect of recombinant Gal-3 carbohydrate recognition domain (Gal3C) in experimental endometriosis treatment. Experimental endometriosis was induced in WT and Gal-3-/- mice. Initially developed lesions were macroscopically and histologically analyzed, including immunohistochemical analysis. Then, WT mice were treated with Gal3C for 15 days. Gal-3 deficiency and Gal3C treatment significantly impaired endometriosis development. A significant decrease in lesions implantation and size, VEGF and VEGFR-2 expression, vascular density and macrophage distribution were observed in Gal-3 absence or inhibition. A greater presence of iNOS positive cells was observed in knockout mice lesions, while the presence of Arginase positive cells was higher in the WT animal lesions. In addition, COX-2 and TGFb1 were reduced by Gal3C treatment. Data showed here indicate a relevant role of Gal-3 in endometriosis development and highlight a target of endometriosis treatment using Gal-3 inhibitor.

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Condition tags

endometriosis

MeSH descriptors

Endometriosis Endometriosis Galectin 3 Molecular Targeted Therapy Animals Biomarkers Biomarkers Endometriosis Endometrium Endometrium Endometrium Female Galectin 3 Galectin 3 Inflammation Inflammation Macrophages Macrophages Macrophages Mice, Inbred BALB C

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europepmc
last seen: 2026-07-29T06:27:48.050232+00:00
openalex
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pubmed
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