Neutrophil gelatinase-associated lipocalin (NGAL) has recently become established as an important contributor to the pathophysiology of cardiovascular disease. Accordingly, it is now viewed as an attractive candidate as a biomarker for various disease states, and in particular has recently become regarded as one of the best diagnostic biomarkers available for acute kidney injury. Nevertheless, the precise physiological effects of NGAL on the heart and the significance of their alterations during the development of heart failure are only now beginning to be characterized. Furthermore, the mechanisms via which NGAL mediates its effects are unclear because there is no conventional receptor signalling pathway. Instead, previous work suggests that regulation of iron metabolism could represent an important mechanism of NGAL action, with wide-ranging consequences spanning metabolic and cardiovascular diseases to host defence against bacterial infection. In the present review, we summarize rapidly emerging evidence for the role of NGAL in regulating heart failure. In particular, we focus on iron transport as a mechanism of NGAL action and discuss this in the context of the existing strong associations between iron overload and iron deficiency with cardiomyopathy.

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