Abstract

ABSTRACT Introduction Diabetes mellitus, a chronic disorder with persistent hyperglycemia, severely affects the quality of life through significant neurological impairments, including neuropathy and cognitive dysfunction. Inflammation and oxidative stress are key factors in these complications, and Lipocalin-2 (LCN2), which is involved in inflammation and iron homeostasis, is crucial in these processes. Area covered This review explores the potential of LCN2 as a therapeutic target for mitigating diabetes neurological complications. By examining the mechanisms by which LCN2 contributes to neuroinflammation, we discuss the therapeutic strategies that target LCN2 to alleviate diabetic neuropathy and cognitive dysfunction. Expert opinion To fully grasp the impact of LCN2 on neurological health, it is essential to understand its multifaceted role in metabolic regulation. Because effective LCN2-targeting drugs must penetrate the blood – brain barrier, various strategies are being developed to meet this requirement. Such therapeutics could treat various neurological complications, including diabetic encephalopathy, retinopathy, and peripheral neuropathy. While animal models offer insights into pathophysiology and potential treatments, their limitations must be acknowledged. Therefore, future research should bridge the gaps between animal findings, human studies, and clinical applications. Moreover, comprehensive personalized approaches, including LCN2-targeting drugs, lifestyle changes, and regularly monitoring individual patients, may be required to manage diabetic complications.

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