Please use this identifier to cite or link to this item: https://repositorio.uca.edu.ar/handle/123456789/11624
Título : Contribution of TRPC channels in neuronal excitotoxicity associated with neurodegenerative disease and ischemic stroke
Autor : Jeon, Jaepyo 
Bu, Fan 
Sun, Guanghua 
Tian, Jin-Bin 
Ting, Shun-Ming 
Li, Jun 
Aronowski, Jaroslaw 
Birnbaumer, Lutz 
Freichel, Marc 
Zhu, Michael X. 
Palabras clave : TRCPFISIOPATOLOGÍAENFERMEDADES NEURODEGENERATIVASACCIDENTE CEREBROVASCULARLESION CEREBRAL
Fecha de publicación : 2021
Editorial : Lausanne: Frontiers Media
Cita : Jeon, J., et al. Contribution of TRPC channels in neuronal excitotoxicity associated with neurodegenerative disease and ischemic stroke [en línea]. Frontiers in cell and developmental biology. 2021, 8. doi: 10.3389/fcell.2020.618663. Disponible en: https://repositorio.uca.edu.ar/handle/123456789/11624
Resumen : Abstract: The seven canonical members of transient receptor potential (TRPC) proteins form cation channels that evoke membrane depolarization and intracellular calcium concentration ([Ca2C]i) rise, which are not only important for regulating cell function but their deregulation can also lead to cell damage. Recent studies have implicated complex roles of TRPC channels in neurodegenerative diseases including ischemic stroke. Brain ischemia reduces oxygen and glucose supply to neurons, i.e., Oxygen and Glucose Deprivation (OGD), resulting in [Ca2C]i elevation, ion dyshomeostasis, and excitotoxicity, which are also common in many forms of neurodegenerative diseases. Although ionotropic glutamate receptors, e.g., N-methyl-D-aspartate receptors, are well established to play roles in excitotoxicity, the contribution of metabotropic glutamate receptors and their downstream effectors, i.e., TRPC channels, should not be neglected. Here, we summarize the current findings about contributions of TRPC channels in neurodegenerative diseases, with a focus on OGD-induced neuronal death and rodent models of cerebral ischemia/reperfusion. TRPC channels play both detrimental and protective roles to neurodegeneration depending on the TRPC subtype and specific pathological conditions involved. When illustrated the mechanisms by which TRPC channels are involved in neuronal survival or death seem differ greatly, implicating diverse and complex regulation. We provide our own data showing that TRPC1/C4/C5, especially TRPC4, may be generally detrimental in OGD and cerebral ischemia/reperfusion. We propose that although TRPC channels significantly contribute to ischemic neuronal death, detailed mechanisms and specific roles of TRPC subtypes in brain injury at different stages of ischemia/reperfusion and in different brain regions need to be carefully and systematically investigated.
URI : https://repositorio.uca.edu.ar/handle/123456789/11624
ISSN : 2296-634X (on line)
Disciplina: MEDICINA
DOI: 10.3389/fcell.2020.618663
Derechos: Acceso abierto
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