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Dementia accompanied by memory loss is considered one of the most common neurodegenerative diseases worldwide, and its prevalence is gradually increasing. Known risk factors for dementia include genetic background, certain lifestyle and dietary patterns, smoking, iron overload, insulin resistance, and impaired glucose metabolism in the brain. Here, we review recent evidence on the regulatory role of lipocalin 2 (LCN2) in dementia from various perspectives. LCN2 is a neutrophil gelatinase-associated protein that influences diverse cellular processes, including the immune system, iron homeostasis, lipid metabolism, and inflammatory responses. Although its functions within the peripheral system are most widely recognized, recent findings have revealed links between LCN2 and central nervous system diseases, as well as novel roles for LCN2 in neurons and glia. Furthermore, LCN2 may modulate diverse pathological mechanisms involved in dementia. Taken together, LCN2 is a promising therapeutic target with which to address the neuropathology of dementia.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8265939 | PMC |
http://dx.doi.org/10.1111/cns.13653 | DOI Listing |
Oncogene
September 2025
Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.
There are no proven therapies for metastatic or unresectable Chromophobe Renal Cell Carcinoma (ChRCC). ChRCC is characterized by high glutathione levels and hypersensitivity to ferroptosis, an iron-dependent form of cell death characterized by peroxidation of polyunsaturated fatty acids. The underlying mechanisms leading to ferroptosis hypersensitivity are unknown.
View Article and Find Full Text PDFTrends Pharmacol Sci
September 2025
Department of Internal Medicine II, Infectious Diseases, Immunology, Rheumatology, Medical University of Innsbruck, Innsbruck, Austria.
The escalating threat of antimicrobial resistance demands innovative therapeutic strategies beyond classical targets. Recent insights into the mechanisms of bacterial iron acquisition - ranging from siderophores and heme uptake to ferrous iron transport - have enabled new approaches to impair pathogen growth and virulence. These pathways are increasingly being harnessed for therapeutic gain.
View Article and Find Full Text PDFBlood Rev
August 2025
Department of Medicine, Stellenbosch University, Faculty of Medicine and Health Sciences, Tygerberg Campus, South Africa. Electronic address:
Clinicians need a good understanding of available tools to diagnose iron deficiency (ID). Interpretation of commonly used laboratory tests can be challenging due to the dynamic nature of iron homeostasis and concurrent inflammation, which influence results. The misinterpretation of iron studies, inconsistencies in ID diagnostic guidelines, and low awareness of non-anaemic ID may lead to missed diagnoses and opportunities for treatment.
View Article and Find Full Text PDFBiochim Biophys Acta Mol Cell Res
September 2025
University of Warsaw, Faculty of Biology, Institute of Experimental Plant Biology and Biotechnology, Department of Plant Metal Homeostasis, 1 Miecznikowa Str., 02-096, Warszawa, Poland. Electronic address:
The Natural Resistance Associated Macrophage Proteins (NRAMPs) are membrane-targeted transporters with low substrate specificity, that mediate the import (translocation to the cytoplasm) of metals, mainly essential nutrients, e.g. iron (Fe), manganese (Mn), zinc (Zn), cobalt (Co), copper (Cu) or nickel (Ni).
View Article and Find Full Text PDFAm J Hematol
September 2025
Nephrology Division and Endocrine Unit, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, USA.
The bone morphogenetic protein (BMP)-SMAD signaling pathway is central to regulating hepcidin, the master regulator of systemic iron homeostasis. We have previously demonstrated that BMP6, BMP2, and, to a lesser extent, BMP5 are the major ligands contributing to hepcidin and iron homeostasis regulation in vivo. Hemojuvelin (HJV) and homeostatic iron regulator (HFE) are hepcidin modulators that are mutated in hereditary hemochromatosis.
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