Document Detail

Galectin-3: an emerging all-out player in metabolic disorders and their complications.
MedLine Citation:
PMID:  25303959     Owner:  NLM     Status:  Publisher    
Galectin-3 has been increasingly recognized as an important modulator of several biological functions, by interacting with several molecules inside and outside the cell, and an emerging player in numerous disease conditions. Galectin-3 exerts various and sometimes contrasting effects according to its location, type of injury, or site of damage. Strong evidence indicates that galectin-3 participates in the pathogenesis of diabetic complications via its receptor function for advanced glycation (AGE) and lipoxidation (ALE) end-products. AGEs/ALEs are produced to an increased extent in target organs of complications, such as kidney and vessels; here, lack of galectin-3 impairs their removal, leading to accelerated damage. In contrast, in the liver, AGE/ALE tissue content and injury are decreased, because lack of galectin-3 results in reduced uptake and tissue accumulation of these by-products. Some of these effects can be explained by changes in the expression of receptor for AGEs (RAGE), associated with galectin-3 deletion and consequent changes in AGE/ALE tissues levels. Furthermore, galectin-3 might exert AGE/ALE- and RAGE-independent effects, favoring resolution of inflammation and modulating fibrogenesis and ectopic osteogenesis. These effects are mediated by intracellular and extracellular galectin-3, the latter via interaction with N-glycans at the cell surface to form lattice structures. Recently, galectin-3 has been implicated in the development of metabolic disorders because it favors glucose homeostasis and prevents the deleterious activation of adaptive and innate immune response to obesogenic/diabetogenic stimuli. In conclusion, galectin-3 is an emerging all-out player in metabolic disorders and their complications that deserves further investigation as potential target of therapeutic intervention.
Giuseppe Pugliese; Carla Iacobini; Carlo M Pesce; Stefano Menini
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Publication Detail:
Type:  REVIEW     Date:  2014-10-9
Journal Detail:
Title:  Glycobiology     Volume:  -     ISSN:  1460-2423     ISO Abbreviation:  Glycobiology     Publication Date:  2014 Oct 
Date Detail:
Created Date:  2014-10-11     Completed Date:  -     Revised Date:  2014-10-12    
Medline Journal Info:
Nlm Unique ID:  9104124     Medline TA:  Glycobiology     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
Copyright Information:
© The Author 2014. Published by Oxford University Press. All rights reserved. For permissions, please e-mail:
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