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The regulation of inflammation by galectin-3

期刊

IMMUNOLOGICAL REVIEWS
卷 230, 期 -, 页码 160-171

出版社

WILEY
DOI: 10.1111/j.1600-065X.2009.00794.x

关键词

galectin-3; inflammation; neutrophil; macrophage; fibrosis; myofibroblast

资金

  1. Wellcome Trust
  2. Medical Research Council [G9900991B] Funding Source: researchfish

向作者/读者索取更多资源

Galectin-3 is a beta-galactoside-binding animal lectin of appro- ximately 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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