Galectins in Atherosclerotic Disease

被引：34

作者：

Al-Ansari, Sali ^{[1
]}

Zeebregts, Clark J. ^{[1
]}

Slart, Riemer H. J. A. ^{[1
]}

Peppelenbosch, Maikel ^{[1
]}

Tio, Rene A. ^{[1
]}

机构：

[1] Univ Groningen, Dept Cell Biol, Univ Med Ctr Groningen, Cardiovasc Imaging Grp Groningen, NL-9713 AV Groningen, Netherlands

来源：

TRENDS IN CARDIOVASCULAR MEDICINE | 2009年 / 19卷 / 05期

关键词：

GLYCATION END-PRODUCTS; SMOOTH-MUSCLE-CELLS; MYOCARDIAL-INFARCTION; EPITHELIAL-CELLS; DEFICIENT MICE; EXPRESSION; GENE; ANGIOGENESIS; LECTIN; PROLIFERATION;

D O I：

10.1016/j.tcm.2009.10.001

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

Although cells constantly adapt to external humoral cues, like cytokines and hormones, in practice, most cellular behavior is under locally guided control, via cell-cell interactions. The most prominent members of this group of molecules involved in this intercellular signaling are the galectins, a family of carbohydrate-binding proteins, which by binding specific receptors induce signaling. It has become clear that galectins are important in the pathogenesis of cardiovascular disease, in particular atherosclerosis, stroke, myocardial infarction, and heart failure. Modulation of galectin signaling holds great promise for the treatment of cardiovascular disease as evident from preclinical studies. (Trends Cardiovasc Med 2009;19:164-169) (C) 2009, Elsevier Inc.

引用

页码：164 / 169

页数：6

共 56 条

[1] Galectin-3 gene (LGALS3) expression in experimental atherosclerosis and cultured smooth muscle cells [J].