Galectin-3: A Central Regulator of Chronic Inflammation and Tissue Fibrosis

Neil C. Henderson, Alison C. Mackinnon, Claire Rooney, Tariq Sethi

Research output: Chapter in Book/Report/Conference proceedingConference contribution

Abstract

Fibrosis is a major cause of morbidity and mortality worldwide. Tissue injury, with chronic inflammation and fibrogenesis, results in disruption of tissue architecture and eventually organ failure. Currently, the therapeutic options for tissue fibrosis are severely limited and organ transplantation is often the only effective treatment for end-stage fibrotic diseases. However, demand for donor organs greatly outstrips supply, and so effective anti-fibrotic treatments are urgently required. In recent years, Galectin-3 has gained prominence as a central regulator of chronic inflammation and fibrogenesis. Tissue fibrosis models in multiple organs have demonstrated that galectin-3 has profound effects on organ fibrogenesis and scarring. In this review we will examine the ways in which galectin-3 regulates these processes through both direct effects on tissue myofibroblasts and also by mediating cross talk between the innate immune system and fibroblast populations in various organs. Additionally, we will discuss how the manipulation of galectin-3 using small molecule inhibitors may have clinical utility in the treatment of patients with a broad range of fibrotic diseases.

Original languageEnglish
Title of host publicationGALECTINS AND DISEASE IMPLICATIONS FOR TARGETED THERAPEUTICS
EditorsAA Klyosov, PG Traber
Place of PublicationWASHINGTON
PublisherAmerican Chemical Society
Pages377-390
Number of pages14
ISBN (Print)978-0-8412-2880-1
Publication statusPublished - 2012
EventSymposium on Galectin Function and Therapeutics - Boston, Morocco
Duration: 17 Sep 201219 Sep 2012

Publication series

NameACS Symposium Series
PublisherAMER CHEMICAL SOC
Volume1115
ISSN (Print)0097-6156

Conference

ConferenceSymposium on Galectin Function and Therapeutics
CountryMorocco
CityBoston
Period17/09/1219/09/12

Keywords

  • TGF-BETA
  • MURINE MODEL
  • ATHEROSCLEROTIC LESIONS
  • GENE-THERAPY
  • CELL-ADHESION
  • RENAL FIBROSIS
  • MODIFIED CITRUS PECTIN
  • AIRWAY INFLAMMATION
  • IDIOPATHIC PULMONARY-FIBROSIS
  • CARBOHYDRATE-BINDING PROTEIN

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