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Academia Mexicana de Neurología, A.C.

2006, Número 1

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Rev Mex Neuroci 2006; 7 (1)


Regulación génica-apoptosis vía p38 en procesos de neuroexcitotoxicidad

Segura TJE, Flores SME, Román RF

Idioma: Español
Referencias bibliográficas: 54
Paginas: 55-68
Archivo PDF: 230.61 Kb.


RESUMEN

En diversos estudios se ha demostrado que el GMS induce dos tipos de muerte celular: una muerte rápida de tipo necrótico, lo cual produce la liberación de neurotransmisores excitatorios como glutamato y GABA (en edad posnatal), esto a su vez desencadena un segundo tipo de muerte celular por apoptosis (muerte retardada), que eventualmente conduce a la activación de la vía MAPKs. De las cuales se conocen tres principales vías que son: ERK, JNK y p38. Éstas promueven la activación de genes tempranos, que bajo condiciones de estrés producen alteraciones en los perfiles de los factores de trascripción, y por lo tanto, alteraciones en la expresión génica. Por lo tanto, es importante conocer la participación de la vía p38, en neuroexcitotoxicidad, lo que puede asociarse con posibles cambios en los niveles de expresión de genes tempranos que se relacionan con el proceso de muerte celular apoptótica; la identificación de estos genes responsables (participantes) en el proceso de muerte celular puede contribuir al diseño de nuevas estrategias terapéuticas para prevenir la neuroexcitotoxicidad, fenómeno común en diversas enfermedades neurodegenerativas crónicas.


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