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Open AccessJournal ArticleDOI

The Role of Galectins as Modulators of Metabolism and Inflammation.

TLDR
Information on galectin-1, -2, -3, -4, -7, -8, -9, and -12 can all induce T-cell apoptosis and modulate inflammation and the potential to target galectins for therapeutic purposes is presented.
Abstract
Galectins are β-galcotosid-binding lectins. The function of galectins varies with their tissue-specific and subcellular location, and their binding to carbohydrates makes them key players in several intra- and extracellular processes where they bind to glycosylated proteins and lipids. In humans, there are 12 identified galectins, some with tissue-specific distribution. Galectins are found inside cells and in the nucleus, cytosol, and organelles, as well as extracellularly. Galectin-1, -2, -3, -4, -7, -8, -9, and -12 can all induce T-cell apoptosis and modulate inflammation. In the context of metabolic control and loss of the same in, for example, diabetes, galectin-1, -2, -3, -9, and -12 are especially interesting. This review presents information on galectins relevant to the control of inflammation and metabolism and the potential to target galectins for therapeutic purposes.

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Intracellular Neutrophil Oxidants: From Laboratory Curiosity to Clinical Reality.

TL;DR: Experimental data and description of a novel chronic granulomatous disease subtype imply that ROS generated in intracellular compartments are key for NETosis and for controlling inflammatory signaling.
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Gene expression profiling of the early pathogenesis of wooden breast disease in commercial broiler chickens using RNA-sequencing.

TL;DR: It is revealed that presence of molecular perturbations involving the vasculature, extracellular matrix and metabolism are pertinent to the onset and early pathogenesis of WBD in commercial meat-type chickens.
Journal ArticleDOI

Extracellular Vesicles as Mediators of Cellular Crosstalk Between Immune System and Kidney Graft.

TL;DR: In conclusion, EVs sustain an intricate crosstalk between graft tissue and innate/adaptive immune systems and are promising as biomarkers and therapeutic tools in KT.
References
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Journal ArticleDOI

Dimeric Galectin-8 induces phosphatidylserine exposure in leukocytes through polylactosamine recognition by the C-terminal domain.

TL;DR: Gal-8 dimerization promotes functional bivalency of each CRD, which allows Gal-8 to signal PS exposure in leukocytes entirely through C-terminal domain recognition of polyLacNAc glycans.
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Galectin-1 receptors in different cell types.

TL;DR: This review will focus on galectin-1 receptors, and some of the mechanisms by which this lectin affects different cell types.
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Galectin-3 regulates mitochondrial stability and antiapoptotic function in response to anticancer drug in prostate cancer.

TL;DR: Findings indicate that Gal-3 inhibits anticancer drug-induced apoptosis through regulation of Bad protein and suppression of the mitochondrial apoptosis pathway, which could improve the efficacy of anticancer drugs chemotherapy in prostate cancer.
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Randomised clinical study: GR-MD-02, a galectin-3 inhibitor, vs. placebo in patients having non-alcoholic steatohepatitis with advanced fibrosis.

TL;DR: Pre‐clinical results of GR‐MD‐02, a galectin‐3 inhibitor, suggested potential efficacy in NASh with advanced fibrosis/cirrhosis and prompted initiation of a clinical development programme in NASH withAdvanced fibrosis.
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Ligand induced galectin-3 protein self-association.

TL;DR: This type-C self-association is named to distinguish it from the previously proposed models (type-N) where galectin-3 molecules bind to each other through the N-terminal domain, and all carbohydrate recognition sites are available for binding glycans.
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