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Galectin‐3: a novel mediator of heart failure development and progression
Author(s) -
Boer Rudolf A.,
Voors Adriaan A.,
Muntendam Pieter,
Gilst Wiek H.,
Veldhuisen Dirk J.
Publication year - 2009
Publication title -
european journal of heart failure
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.149
H-Index - 133
eISSN - 1879-0844
pISSN - 1388-9842
DOI - 10.1093/eurjhf/hfp097
Subject(s) - galectin 3 , medicine , heart failure , fibrosis , galectin , inflammation , mediator , pathophysiology , disease , myocardial fibrosis , cancer , cardiac fibrosis , bioinformatics , immunology , biology
Galectins are a family of soluble β ‐galactoside‐binding lectins that play many important regulatory roles in inflammation, immunity, and cancer. Recently, a role for galectin‐3 in the pathophysiology of heart failure (HF) has been suggested. Numerous studies have demonstrated the up‐regulation of galectin‐3 in hypertrophied hearts, its stimulatory effect on macrophage migration, fibroblast proliferation, and the development of fibrosis. The latter observation is particularly relevant as cardiac remodelling is an important determinant of the clinical outcome of HF and is linked to disease progression and poor prognosis. Because galectin‐3 expression is maximal at peak fibrosis and virtually absent after recovery, routine measurement in patients with HF may prove valuable to identify those patients at highest risk for readmission or death, thus enabling physicians to tailor the level of care to individual patient needs. This review summarizes the most recent advances in galectin‐3 research, with an emphasis on the role galectin‐3 plays in the development and progression of HF.