Format

Send to

Choose Destination
See comment in PubMed Commons below
Front Endocrinol (Lausanne). 2013 Jan 22;3:179. doi: 10.3389/fendo.2012.00179. eCollection 2012.

Association of intercellular adhesion molecule 1 (ICAM1) with diabetes and diabetic nephropathy.

Author information

1
M1:03 Rolf Luft Center for Diabetes and Endocrinology Research, Department of Molecular Medicine and Surgery, Karolinska Institutet, Karolinska University Hospital Stockholm, Sweden.

Abstract

Diabetes and diabetic nephropathy are complex diseases affected by genetic and environmental factors. Identification of the susceptibility genes and investigation of their roles may provide useful information for better understanding of the pathogenesis and for developing novel therapeutic approaches. Intercellular adhesion molecule 1 (ICAM1) is a cell surface glycoprotein expressed on endothelial cells and leukocytes in the immune system. The ICAM1 gene is located on chromosome 19p13 within the linkage region of diabetes. In the recent years, accumulating reports have implicated that genetic polymorphisms in the ICAM1 gene are associated with diabetes and diabetic nephropathy. Serum ICAM1 levels in diabetes patients and the icam1 gene expression in kidney tissues of diabetic animals are increased compared to the controls. Therefore, ICAM1 may play a role in the development of diabetes and diabetic nephropathy. In this review, we present genomic structure, variation, and regulation of the ICAM1 gene, summarized genetic and biological studies of this gene in diabetes and diabetic nephropathy and discussed about the potential application using ICAM1 as a biomarker and target for prediction and treatment of diabetes and diabetic nephropathy.

KEYWORDS:

diabetic nephropathy; end-stage renal disease; intercellular adhesion molecule 1; type 1 diabetes mellitus; type 2 diabetes mellitus

PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Frontiers Media SA Icon for PubMed Central
    Loading ...
    Support Center