The process of generating new functional neurons in the adult mammalian brain occurs from the local neural stem and progenitor cells and requires tight control of the progenitor cell's activity. Several signaling pathways and intrinsic/extrinsic factors have been well studied over the last years, but recent attention has been given to the critical role of cellular metabolism in determining the functional properties of progenitor cells. Here, we review recent advances in the current understanding of when and how metabolism affects neural stem cell (NSC) behavior and subsequent neuronal differentiation and highlight the role of lipocalin-2 (LCN2), a protein involved in the control of oxidative stress, as a recently emerged regulator of NSC activity and neuronal differentiation.
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| http://dx.doi.org/10.1016/j.neubiorev.2018.09.014 | DOI Listing |
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Evaluation of the serum level of Lipocalin 2 in vitiligo.
Arch Dermatol Res
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Department of Dermatology, Faculty of Medicine, Fayoum University, Fayoum, Egypt.
Vitiligo is considered as depigmenting skin disorder where patches of skin losing their pigment. Lipocalin-2 (LCN2) is one of the Inflammatory adipokines that has a potential role in skin disorders and other inflammatory diseases as well. To measure the concentration level of LCN2 in vitiligo patients compared to healthy controls and to investigate its relation to disease activity and other clinical data to evaluate its role in the pathogenesis of the disease.
View Article and Find Full Text PDFAdipose tissue may not be a major player in the inflammatory pathogenesis of Autism Spectrum Disorder.
Brain Behav Immun Health
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Institute of Maternal and Child Medicine, Shenzhen Maternity and Child Healthcare Hospital, Southern Medical University, Shenzhen, China.
Purpose: Autism spectrum disorder (ASD) is a complex neurodevelopmental disorder increasingly recognized for its strong association with chronic inflammation. Adipose tissue functions as an endocrine organ and can secrete inflammatory cytokines to mediate inflammation. However, its involvement in ASD-related inflammation remains unclear.
View Article and Find Full Text PDFLCN2 blockade mitigating metabolic dysregulation and redefining appetite control in type 2 diabetes.
Metab Brain Dis
January 2025
Section of Osteimmunology and Oral Immunology, Laboratory of Dental Reseach. FES Iztacala, National Autonomous University of Mexico (UNAM), México, Mexico State, México.
Unlabelled: LCN2 has an osteokine important for appetite regulation; in type 2 diabetes (T2D) it is not known whether appetite regulation mediated by LCN2 in the brain is altered. In this work, we focus on exploring the role of blocking LCN2 in metabolic health and appetite regulation within the central nervous system of mice with T2D.
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J Orthop Translat
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Article Synopsis
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IRF7 Activates LCN2 Transcription to Enhance LPS-Induced Acute Lung Injury by Inducing Macrophage Ferroptosis and M1 Polarization.
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Department of Respiratory and Critical Care Medicine, Lishui Second People's Hospital, Lishui, China.
Acute lung injury (ALI), a severe pulmonary disorder that poses a significant threat to life, is closely associated with macrophage ferroptosis and polarization. Lipocalin 2 (LCN2) has been previously reported to be implicated in the pathogenesis of ALI. However, the specific role of LCN2 in macrophage ferroptosis and polarization remains undetermined.
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