Fig. 2

The roles and mechanisms of NGAL in ischemic heart disease. NGAL interacted with MMP-9 to increase plaque vulnerability. NGAL has two receptors, the 24p3R, and the megalin receptor. NGAL participates in controlling iron homeostasis, the activation of pro-inflammatory and pro-fibrosis signaling pathways through 24p3R. However, the role of the NGAL-megalin complex has not been well described. NGAL induced the proliferation of human vascular SMC and cardiac fibroblasts, which promoted the development of atherosclerosis and thus the occurrence of myocardial infarction. In addition, NGAL participates in ischemic heart disease by apoptosis, autophagy, and the Erk1/2 pathway. Abridgment NGAL is short for Neutrophil gelatinase-associated lipocalin; MMP-9 is short for matrix metalloproteinases 9; 24p3R is short for 24p3 receptor; ERK1/2 is short for extracellular regulated protein kinases 1/2; NF-κB is short for nuclear factor kappa-B; IκB is short for Inhibitor kappa B; TGF-β is short for Transforming growth factor β; MI is short for myocardial infarction; SMC is short for the smooth muscle cell. The question mark (?) indicates that some discrepancy still exists