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半乳糖凝集素-3 在心血管疾病中的作用。

Galectin-3 in Cardiovascular Diseases.

机构信息

Dipartimento di Medicina Molecolare e Biotecnologie Mediche, Università degli Studi di Napoli Federico II, 80131 Naples, Italy.

Istituto Zooprofilattico Sperimentale della Sicilia, via Gino Marinuzzi 3, 90129 Palermo, Italy.

出版信息

Int J Mol Sci. 2020 Dec 3;21(23):9232. doi: 10.3390/ijms21239232.

DOI:10.3390/ijms21239232
PMID:33287402
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7731136/
Abstract

Galectin-3 (Gal-3) is a β-galactoside-binding protein belonging to the lectin family with pleiotropic regulatory activities and several physiological cellular functions, such as cellular growth, proliferation, apoptosis, differentiation, cellular adhesion, and tissue repair. Inflammation, tissue fibrosis and angiogenesis are the main processes in which Gal-3 is involved. It is implicated in the pathogenesis of several diseases, including organ fibrosis, chronic inflammation, cancer, atherosclerosis and other cardiovascular diseases (CVDs). This review aims to explore the connections of Gal-3 with cardiovascular diseases since they represent a major cause of morbidity and mortality. We herein discuss the evidence on the pro-inflammatory role of Gal-3 in the atherogenic process as well as the association with plaque features linked to lesion stability. We report the biological role and molecular mechanisms of Gal-3 in other CVDs, highlighting its involvement in the development of cardiac fibrosis and impaired myocardium remodelling, resulting in heart failure and atrial fibrillation. The role of Gal-3 as a prognostic marker of heart failure is described together with possible diagnostic applications to other CVDs. Finally, we report the tentative use of Gal-3 inhibition as a therapeutic approach to prevent cardiac inflammation and fibrosis.

摘要

半乳糖凝集素-3(Gal-3)是一种属于凝集素家族的β-半乳糖苷结合蛋白,具有多种调节活性和几种生理细胞功能,如细胞生长、增殖、凋亡、分化、细胞黏附和组织修复。炎症、组织纤维化和血管生成是 Gal-3 参与的主要过程。它与包括器官纤维化、慢性炎症、癌症、动脉粥样硬化和其他心血管疾病(CVDs)在内的多种疾病的发病机制有关。本综述旨在探讨 Gal-3 与心血管疾病的联系,因为它们是发病率和死亡率的主要原因。我们在此讨论 Gal-3 在动脉粥样硬化过程中的促炎作用以及与斑块特征相关的病变稳定性的证据。我们报告了 Gal-3 在其他 CVDs 中的生物学作用和分子机制,强调了其在心包纤维化和受损心肌重塑发展中的作用,导致心力衰竭和心房颤动。描述了 Gal-3 作为心力衰竭预后标志物的作用以及对其他 CVDs 的可能诊断应用。最后,我们报告了 Gal-3 抑制作为预防心脏炎症和纤维化的治疗方法的尝试。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8bbf/7731136/4868fabcadbc/ijms-21-09232-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8bbf/7731136/c130052974a6/ijms-21-09232-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8bbf/7731136/4868fabcadbc/ijms-21-09232-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8bbf/7731136/c130052974a6/ijms-21-09232-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8bbf/7731136/4868fabcadbc/ijms-21-09232-g002.jpg

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