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      Galectin-3: One Molecule for an Alphabet of Diseases, from A to Z

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          Abstract

          Galectin-3 (Gal-3) regulates basic cellular functions such as cell–cell and cell–matrix interactions, growth, proliferation, differentiation, and inflammation. It is not surprising, therefore, that this protein is involved in the pathogenesis of many relevant human diseases, including cancer, fibrosis, chronic inflammation and scarring affecting many different tissues. The papers published in the literature have progressively increased in number during the last decades, testifying the great interest given to this protein by numerous researchers involved in many different clinical contexts. Considering the crucial role exerted by Gal-3 in many different clinical conditions, Gal-3 is emerging as a new diagnostic, prognostic biomarker and as a new promising therapeutic target. The current review aims to extensively examine the studies published so far on the role of Gal-3 in all the clinical conditions and diseases, listed in alphabetical order, where it was analyzed.

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          Most cited references386

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          Liver fibrosis.

          Liver fibrosis is the excessive accumulation of extracellular matrix proteins including collagen that occurs in most types of chronic liver diseases. Advanced liver fibrosis results in cirrhosis, liver failure, and portal hypertension and often requires liver transplantation. Our knowledge of the cellular and molecular mechanisms of liver fibrosis has greatly advanced. Activated hepatic stellate cells, portal fibroblasts, and myofibroblasts of bone marrow origin have been identified as major collagen-producing cells in the injured liver. These cells are activated by fibrogenic cytokines such as TGF-beta1, angiotensin II, and leptin. Reversibility of advanced liver fibrosis in patients has been recently documented, which has stimulated researchers to develop antifibrotic drugs. Emerging antifibrotic therapies are aimed at inhibiting the accumulation of fibrogenic cells and/or preventing the deposition of extracellular matrix proteins. Although many therapeutic interventions are effective in experimental models of liver fibrosis, their efficacy and safety in humans is unknown. This review summarizes recent progress in the study of the pathogenesis and diagnosis of liver fibrosis and discusses current antifibrotic strategies.
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            Fibrotic disease and the T(H)1/T(H)2 paradigm.

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              Galectins as modulators of tumour progression.

              Galectins are a family of animal lectins with diverse biological activities. They function both extracellularly, by interacting with cell-surface and extracellular matrix glycoproteins and glycolipids, and intracellularly, by interacting with cytoplasmic and nuclear proteins to modulate signalling pathways. Current research indicates that galectins have important roles in cancer; they contribute to neoplastic transformation, tumour cell survival, angiogenesis and tumour metastasis. They can modulate the immune and inflammatory responses and might have a key role helping tumours to escape immune surveillance. How do the different members of the Galectin family contribute to these diverse aspects of tumour biology?
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                Author and article information

                Journal
                Int J Mol Sci
                Int J Mol Sci
                ijms
                International Journal of Molecular Sciences
                MDPI
                1422-0067
                26 January 2018
                February 2018
                : 19
                : 2
                : 379
                Affiliations
                [1 ]Department of Clinical and Molecular Medicine, Sapienza University, Policlinico Umberto I, Viale Regina Elena 324, 00161 Rome, Italy; alberto.ricci@ 123456uniroma1.it
                [2 ]Laboratory of Biomedical Research, Niccolò Cusano University Foundation, Via Don Carlo Gnocchi 3, 00166 Rome, Italy; luca.lavra@ 123456fondazioneniccolocusano.it (L.L.); alessandra.morgante@ 123456fondazioneniccolocusano.it (A.M.); alessandra.ulivieri@ 123456fondazioneniccolocusano.it (A.U.); fiorenza.magi@ 123456fondazioneniccolocusano.it (F.M.); leila.b.salehi@ 123456fondazioneniccolocusano.it (L.B.S.)
                [3 ]Department of Oncological Science, Breast Unit, St Andrea University Hospital, Via di Grottarossa, 1035/39, 00189 Rome, Italy; Gianpaolo.defrancesco@ 123456gmail.com
                [4 ]Operative Unit Surgery of Thyroid and Parathyroid, Sapienza University of Rome, S. Andrea Hospital, Via di Grottarossa, 1035/39, 00189 Rome, Italy; carlo_bellotti@ 123456hotmail.com
                [5 ]Department of Biopathology and Diagnostic Imaging, Tor Vergata University, Via Montpellier 1, 00133 Rome, Italy
                Author notes
                [* ]Correspondence: salvatore.sciacchitano@ 123456fondazioneniccolocusano.it ; Tel.: +39-06-4567-8373
                Article
                ijms-19-00379
                10.3390/ijms19020379
                5855601
                29373564
                59951ff3-7925-463b-b64e-10eccbc9853a
                © 2018 by the authors.

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                : 31 December 2017
                : 22 January 2018
                Categories
                Review

                Molecular biology
                galectin-3,gal-3
                Molecular biology
                galectin-3, gal-3

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