Galectin-3 is a versatile protein orchestrating several physiological and pathophysiological processes in the human body. In the last decade, considerable interest in galectin-3 has emerged because of its potential role as a biotarget. Galectin-3 is differentially expressed depending on the tissue type, however its expression can be induced under conditions of tissue injury or stress. Galectin-3 overexpression and secretion is associated with several diseases and is extensively studied in the context of fibrosis, heart failure, atherosclerosis and diabetes mellitus. Monomeric (extracellular) galectin-3 usually undergoes further “activation” which significantly broadens the spectrum of biological activity mainly by modifying its carbohydrate-binding properties. Self-interactions of this protein appear to play a crucial role in regulating the extracellular activities of this protein, however there is limited and controversial data on the mechanisms involved. We therefore summarize (recent) literature in this area and describe galectin-3 from a binding perspective providing novel insights into mechanisms by which galectin-3 is known to be “activated” and how such activation may be regulated in pathophysiological scenarios.

中文翻译：

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Galectin-3在心力衰竭和心血管疾病中的激活和抑制作用：最新进展

Galectin-3是一种多功能蛋白质，可调节人体的几种生理和病理生理过程。在过去的十年中，由于半乳凝素3作为生物靶标的潜在作用，人们对半乳凝素3产生了极大的兴趣。Galectin-3的表达取决于组织类型，但是在组织损伤或应激条件下可以诱导其表达。Galectin-3的过表达和分泌与多种疾病有关，并在纤维化，心力衰竭，动脉粥样硬化和糖尿病方面进行了广泛研究。单体（细胞外）半乳凝素3通常会经历进一步的“活化”，这主要是通过改变其与碳水化合物的结合特性来显着拓宽生物活性的范围。这种蛋白质的自我相互作用似乎在调节这种蛋白质的细胞外活性中起着至关重要的作用，但是有关这种机制的数据有限且有争议。因此，我们总结（最近）该领域的文献，并从结合的角度描述galectin-3，从而提供有关galectin-3被“激活”的机制的新见解，以及如何在病理生理情况下调节这种激活。