1. Academic Validation
  2. The regulation of inflammation by galectin-3

The regulation of inflammation by galectin-3

  • Immunol Rev. 2009 Jul;230(1):160-71. doi: 10.1111/j.1600-065X.2009.00794.x.
Neil C Henderson 1 Tariq Sethi
Affiliations

Affiliation

  • 1 Centre for Inflammation Research, The Queen's Medical Research Institute, University of Edinburgh, Edinburgh, UK.
Abstract

Galectin-3 is a beta-galactoside-binding animal lectin of approximately 30 kDa and is evolutionarily highly conserved. Galectin-3 is promiscuous, its localization within the tissue micro-environment may be extracellular, cytoplasmic, or nuclear, and it has a concentration-dependent ability to be monomeric or form oligomers. These properties impart great flexibility on Galectin-3 as a specific regulator of many biological systems including inflammation. For example, in acute tissue damage Galectin-3 is a key component in the host defense against microbes such as Streptococcus pneumoniae. However, if tissue injury becomes repetitive Galectin-3 also appears to be intimately involved in the transition to chronic inflammation, facilitating the walling off of tissue injury with fibrogenesis and organ scarring. Therefore Galectin-3 can be viewed as a regulatory molecule acting at various stages along the continuum from acute inflammation to chronic inflammation and tissue fibrogenesis. In this review, we examine the role of Galectin-3 in inflammation, and discuss the manipulation of Galectin-3 expression as a potentially novel therapeutic strategy in the treatment of a broad range of inflammatory diseases.

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