Elevated serum levels of galectin-3, a member of the lectin family, have recently
been reported in heart failure patients, as well as in animal models of heart failure
[
1
,
2
,
3
]. Apart from cardiac remodelling, upregulation of galectin-3 expression and release
has also been associated with several other human fibrotic conditions including liver
cirrhosis, idiopathic lung fibrosis, pancreatitis and renal failure. Therefore, this
lectin is thought to play some regulatory role between inflammation and fibrosis [
- Sharma U.
- Rhaleb N.E.
- Pokharel S.
- et al.
Novel anti-inflammatory mechanisms of N-Acetyl-Ser-Asp-Lys-Pro in hypertension-induced
target organ damage.
Am J Physiol Heart Circ Physiol. 2008; 294: H1226-H1232
- Conroy R.M.
- Pyörälä K.
- Fitzgerald A.P.
987–1003
Estimation of ten-year risk of fatal cardiovascular disease in Europe: the SCORE project.
Estimation of ten-year risk of fatal cardiovascular disease in Europe: the SCORE project.
Eur Heart J. 2003; 24: 987-1003
[1]
]. Its direct mediation of profibrotic pathways such as cell adhesion and proliferation
suggests that galectin-3 is involved in the development of heart failure [
4
,
5
]. After acute myocardial infarction (AMI), fibrosis and tissue remodelling are the
leading causes for the development of heart failure.Keywords
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References
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Article info
Publication history
Published online: July 16, 2012
Accepted:
June 24,
2012
Received:
May 29,
2012
Identification
Copyright
© 2012 Elsevier Ireland Ltd. Published by Elsevier Inc. All rights reserved.