Piacvezérelt kutatás-fejlesztési és innovációs projektek támogatása(2020-1.1.2-PIACI-KFI-2021-00273)
Támogató: Nemzeti Kutatási, Fejlesztési és Innovációs Hivatal
(2019-2.1.7-ERANET-2020-00014)
ERA PerMed(2020-346 grant) Támogató: EU
Galectins, a family of beta-galactoside-binding proteins, are critical in regulating
feto-maternal interactions during pregnancy. Their evolutionary trajectory is reflected
in their expression patterns and diverse functions in embryo implantation, trophoblast
invasion, and maternal immune and vascular adaptation, contributing to healthy placentation
and uncomplicated pregnancy. Galectin-1 (gal-1), one of the most ancient galectins,
plays a pivotal role in feto-maternal immune regulation, acting predominantly from
the maternal side to promote immune tolerance, a function integrated early in placental
mammalian evolution. In contrast, anthropoid primates introduced a unique set of fetal
(placental) galectins (gal-13, gal-14, and gal-16) through birth-and-death evolution,
with these genes localized on human chromosome 19. Notably, these primate species
have evolved varying degrees of deep placentation, with humans exhibiting the deepest,
which facilitates enhanced nutrient delivery to the fetus, particularly for brain
development. Placental galectins have been implicated in the evolution of immune tolerance
mechanisms that support deep placentation. During pregnancy, reduced expression of
maternal galectins (e.g., gal-1) and placental galectins (e.g., gal-13) has been associated
with severe obstetric complications, signaling disruptions in feto-maternal tolerance.
This review provides a comprehensive overview of gal-1, gal-13, gal-14, and gal-16,
highlighting their shared and unique roles in maternal and placental immune regulation
and placental development. Additionally, the review explores the potential of maternal
versus placental galectins as biomarkers and therapeutic targets to improve diagnostic
and treatment strategies for adverse pregnancy outcomes.
