NOX activation in reactive astrocytes regulates astrocytic LCN2 expression and neurodegeneration
R Liu, J Wang, Y Chen, JM Collier, O Capuk, S Jin… - Cell Death & …, 2022 - nature.com
Reactive astrocytes (RA) secrete lipocalin-2 (LCN2) glycoprotein that regulates diverse
cellular processes including cell death/survival, inflammation, iron delivery and cell …
cellular processes including cell death/survival, inflammation, iron delivery and cell …
Reduced secretion of LCN2 (lipocalin 2) from reactive astrocytes through autophagic and proteasomal regulation alleviates inflammatory stress and neuronal damage
BK Jung, Y Park, B Yoon, JS Bae, SW Han, JE Heo… - Autophagy, 2023 - Taylor & Francis
ABSTRACT LCN2/neutrophil gelatinase-associated lipocalin/24p3 (lipocalin 2) is a
secretory protein that acts as a mammalian bacteriostatic molecule. Under …
secretory protein that acts as a mammalian bacteriostatic molecule. Under …
Lipocalin-2 as a therapeutic target for brain injury: an astrocentric perspective
K Suk - Progress in neurobiology, 2016 - Elsevier
Abstract Lipocalin-2 (LCN2) is a member of the secreted lipocalin protein family. LCN2 is
also a representative gliocalin that is primarily released by glial cells, as well as acts upon …
also a representative gliocalin that is primarily released by glial cells, as well as acts upon …
Lipocalin-2 may produce damaging effect after cerebral ischemia by inducing astrocytes classical activation
N Zhao, X Xu, Y Jiang, J Gao, F Wang, X Xu… - Journal of …, 2019 - Springer
Background Functions of astrocytes in the rehabilitation after ischemic stroke, especially
their impacts on inflammatory processes, remain controversial. This study uncovered two …
their impacts on inflammatory processes, remain controversial. This study uncovered two …
Lipocalin-2 in the inflammatory activation of brain astrocytes
ABSTRACT Lipocalin-2 (LCN2), a secretory protein, regulates diverse cellular processes
such as cell death/survival, cell migration/invasion, cell differentiation, iron delivery …
such as cell death/survival, cell migration/invasion, cell differentiation, iron delivery …
Lipocalin-2: a therapeutic target to overcome neurodegenerative diseases by regulating reactive astrogliosis
BK Jung, KY Ryu - Experimental & Molecular Medicine, 2023 - nature.com
Glial cell activation precedes neuronal cell death during brain aging and the progression of
neurodegenerative diseases. Under neuroinflammatory stress conditions, lipocalin-2 …
neurodegenerative diseases. Under neuroinflammatory stress conditions, lipocalin-2 …
NOX2-mediated reactive oxygen species are double-edged swords in focal cerebral ischemia in mice
Y Yingze, J Zhihong, J Tong, L Yina, Z Zhi, Z Xu… - Journal of …, 2022 - Springer
Background Reactive oxygen species (ROS) often promote acute brain injury after stroke,
but their roles in the recovery phase have not been well studied. We tested the hypothesis …
but their roles in the recovery phase have not been well studied. We tested the hypothesis …
Lipocalin-2 and cerebral stroke
C Luo, S Zhou, S Yin, L Jian, P Luo, J Dong… - Frontiers in molecular …, 2022 - frontiersin.org
Stroke is a common and devastating disease with an escalating prevalence worldwide. The
known secondary injuries after stroke include cell death, neuroinflammation, blood-brain …
known secondary injuries after stroke include cell death, neuroinflammation, blood-brain …
Lipocalin-2 is an autocrine mediator of reactive astrocytosis
Astrocytes, the most abundant glial cell type in the brain, provide metabolic and trophic
support to neurons and modulate synaptic activity. In response to a brain injury, astrocytes …
support to neurons and modulate synaptic activity. In response to a brain injury, astrocytes …
[HTML][HTML] Lipocalin-2 is a key regulator of neuroinflammation in secondary traumatic and ischemic brain injury
Reactive glial cells are hallmarks of brain injury. However, whether these cells contribute to
secondary inflammatory pathology and neurological deficits remains poorly understood …
secondary inflammatory pathology and neurological deficits remains poorly understood …
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