Review of lipocalin-2-mediated effects in diabetic retinopathy.

BACKGROUND: Studies have uncovered LCN2 as a marker of inflammation strongly related to obesity, insulin resistance, and abnormal glucose metabolism in humans, and is involved in vascular diseases, inflammatory diseases, and neurological diseases. In recent years, studies have shown that elevated levels of LCN2 have a strong association with diabetic retinopathy (DR), but the pathogenesis is unknown. Here, we reviewed the relevant literature and compiled the pathogenesis associated with LCN2-induced DR. METHODS: We searched PubMed and Web of Science electronic databases using "lipocalin-2, diabetic retinopathy, retinal degeneration, diabetic microangiopathies, diabetic neuropathy and inflammation" as subject terms. RESULTS: In diabetic retinal neuropathy, LCN2 causes impaired retinal photoreceptor function and retinal neurons; in retinal microangiopathy, LCN2 induces apoptosis of retinal vascular endothelial cells and promotes angiogenesis; in retinal inflammation, increased secretion of LCN2 recruits inflammatory cells and induces pro-inflammatory cytokines. Moreover, LCN2 has the potential as a biomarker for DR. Recent studies have shown that retinal damage can be attenuated by silencing LCN2, which may be associated with the inhibition of caspase-1-mediated pyroptosis, and LCN2 may be a new target for the treatment of DR. CONCLUSIONS: In conclusion, LCN2, involved in the development of diabetic retinopathy, is a key factor in diabetic retinal microangiopathy, neurodegeneration, and retinal inflammation. LCN2 is likely to be a novel molecular target leading to DR, and a more in-depth study of the pathogenesis of DR caused by LCN2 may provide considerable benefits for clinical research and potential drug development.

Association between lipocalin-2 levels and diabetic retinopathy in patients with overweight/obese type 2 diabetes mellitus.

AIMS: The study aimed to investigate the association between lipocalin-2 (LCN-2) levels and diabetic retinopathy (DR) in patients with overweight/obese type 2 diabetes mellitus(T2DM), and to explore the mechanism of LCN-2 in overweight/obese DR. METHODS: The study involved 237 T2DM inpatients divided into the normal group and overweight/obese group, and the two groups were further divided into two subgroups according to the presence or absence of DR. The demographic data and biochemical parameters were measured. RESULTS: LCN-2 levels in overweight/obese groups were higher than those in normal groups (P < 0.001 for all), and patients with DR had higher levels of LCN-2 than those without DR(P < 0.05 for all) in normal groups and overweight/obese groups. Binary logistic regression analysis showed that no significant significance was observed for LCN-2 levels compared to those below the median in the normal group, but individuals with LCN-2 levels above the median had 4.198 times higher risk of developing DR than those below the median (OR = 4.198, 95% CI = 1.676-10.516) after adjustment for potential confounding factors in the overweight/obese group. In the total, normal and overweight/obese groups, the prediction capacity of LCN-2 for DR was 1.56, 1.58 and 1.65 times, respectively. Conclusionsː In conclusion, our study found that LCN-2 levels were higher in overweight/obese patients with DR, and LCN-2 was an independent predictor of DR in T2DM patients with overweight/obese. In addition, LCN-2 may be a valuable predictor of DR-like factors such as the duration of diabetes and hypertension.