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Mostrando ítems 1-6 de 6
Artículo
Caspase signalling controls microglia activation and neurotoxicity
(Springer Nature, 2011-04-11)
Activation of microglia and inflammation-mediated neurotoxicity are suggested to play a decisive role in the pathogenesis of several neurodegenerative disorders. Activated microglia release pro-inflammatory factors that ...
Artículo
Regulation of caspase-3 processing by cIAP2 controls the switch between pro-inflammatory activation and cell death in microglia
(Nature Publishing Group, 2014)
The activation of microglia, resident immune cells of the central nervous system, and inflammation-mediated neurotoxicity are typical features of neurodegenerative diseases, for example, Alzheimer's and Parkinson's diseases. ...
Artículo
Deletion of caspase-8 in mouse myeloid cells blocks microglia pro-inflammatory activation and confers protection in MPTP neurodegeneration model
(Impact Journals, LLC, 2015)
Increasing evidence involves sustained pro-inflammatory microglia activation in the pathogenesis of different neurodegenerative diseases, particularly Parkinson's disease (PD). We recently uncovered a completely novel and ...
Artículo
Glioma-induced inhibition of caspase-3 in microglia promotes a tumor-supportive phenotype
(Springer Nature, 2016-10-19)
Glioma cells recruit and exploit microglia (the resident immune cells of the brain) for their proliferation and invasion ability. The underlying molecular mechanism used by glioma cells to transform microglia into a ...
Artículo
Microglia: Agents of the CNS Pro-Inflammatory Response
(Multidisciplinary Digital Publishing Institute (MDPI), 2020)
The pro-inflammatory immune response driven by microglia is a key contributor to the pathogenesis of several neurodegenerative diseases. Though the research of microglia spans over a century, the last two decades have ...
Artículo
Microglia-secreted galectin-3 acts as a toll-like receptor 4 ligand and contributes to microglial activation
(2015)
Inflammatory response induced by microglia plays a critical role in the demise of neuronal populations in neuroinflammatory diseases. Although the role of toll-like receptor 4 (TLR4) in microglia’s inflammatory response ...