Abstract：
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.
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.
摘要：
背景：研究发现LCN2是与肥胖密切相关的炎症标志物，胰岛素抵抗，人类的葡萄糖代谢异常，与血管疾病有关，炎症性疾病，和神经系统疾病。近年来,研究表明，LCN2水平升高与糖尿病视网膜病变（DR）有很强的相关性，但其发病机制尚不清楚。这里,我们回顾了相关文献并整理了与LCN2诱导的DR相关的发病机制。
方法：我们使用“脂质运载蛋白-2，糖尿病性视网膜病变，视网膜变性,糖尿病微血管病变,糖尿病神经病变和炎症“作为主题词。
结果：在糖尿病性视网膜神经病中，LCN2导致视网膜光感受器功能和视网膜神经元受损；在视网膜微血管病中，LCN2诱导视网膜血管内皮细胞凋亡并促进血管生成；在视网膜炎症中，LCN2分泌增加募集炎性细胞并诱导促炎细胞因子。此外，LCN2具有作为DR生物标志物的潜力。最近的研究表明，沉默LCN2可以减轻视网膜损伤，这可能与抑制caspase-1介导的焦亡有关，LCN2可能是治疗DR的新靶点。
结论：结论：LCN2参与糖尿病视网膜病变的发展，是糖尿病视网膜微血管病变的关键因素，神经变性,和视网膜炎症。LCN2可能是导致DR的新分子靶标，而更深入地研究LCN2引起的DR的发病机制可能为临床研究和潜在药物开发提供可观的益处。
方法：我们使用“脂质运载蛋白-2，糖尿病性视网膜病变，视网膜变性,糖尿病微血管病变,糖尿病神经病变和炎症“作为主题词。
结果：在糖尿病性视网膜神经病中，LCN2导致视网膜光感受器功能和视网膜神经元受损；在视网膜微血管病中，LCN2诱导视网膜血管内皮细胞凋亡并促进血管生成；在视网膜炎症中，LCN2分泌增加募集炎性细胞并诱导促炎细胞因子。此外，LCN2具有作为DR生物标志物的潜力。最近的研究表明，沉默LCN2可以减轻视网膜损伤，这可能与抑制caspase-1介导的焦亡有关，LCN2可能是治疗DR的新靶点。
结论：结论：LCN2参与糖尿病视网膜病变的发展，是糖尿病视网膜微血管病变的关键因素，神经变性,和视网膜炎症。LCN2可能是导致DR的新分子靶标，而更深入地研究LCN2引起的DR的发病机制可能为临床研究和潜在药物开发提供可观的益处。
