Galectin-3 and Fibrosis: Research in the Last 5 Years

I. Eliaz
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引用次数: 2

Abstract

Tissue fibrosis is initially an adaptive response to organ injury, but eventually, parenchymal scarring and subsequent cellular dysfunction and organ failure ensue. Few therapies currently exist for fibrosis, especially those that target fibrogenesis. Galectin-3 (Gal-3) is a member of the lectin family of proteins, is produced predominantly by macrophages, and has essential functions in inflammation and angiogenesis. Gal-3 is activated in fibrotic models and abnormally elevated in fibrotic patients. Gal-3 inhibitors help to ameliorate or prevent fibrosis. For this review, we searched for original articles and reviews published between Jul 1, 2014, and Nov 1, 2019, using the following search terms (or combination of words) in PubMed: “galectin 3”, “fibrosis”, “heart”, “cardiac”, “liver”, “hepatic”, “lung”, “pulmonary”, “kidney”, and “renal”.
半凝集素-3与纤维化:近5年的研究
组织纤维化最初是对器官损伤的适应性反应,但最终,实质瘢痕和随后的细胞功能障碍和器官衰竭随之而来。目前针对纤维化的治疗方法很少,尤其是针对纤维化发生的治疗方法。半乳糖凝集素-3 (Gal-3)是凝集素家族的一员,主要由巨噬细胞产生,在炎症和血管生成中具有重要功能。Gal-3在纤维化模型中被激活,在纤维化患者中异常升高。Gal-3抑制剂有助于改善或预防纤维化。在本综述中,我们检索了2014年7月1日至2019年11月1日期间发表的原创文章和评论,使用PubMed中的以下搜索词(或词的组合):“galectin 3”、“fibrosis”、“heart”、“cardiac”、“liver”、“liver”、“lung”、“pulmonary”、“kidney”和“renal”。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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