Cellular Senescence, Neurological Function, and Redox State


Por: Angel Maciel-Baron, Luis, Moreno-Blas, Daniel, Lizbeth Morales-Rosales, Sandra, Yazmin Gonzalez-Puertos, Viridiana, Edith Lopez-Diazguerrero, Norma, Torres, Claudio, Castro-Obregon, Susana, Konigsberg, Mina

Publicada: 1 jun 2018
Resumen:
Significance: Cellular senescence, characterized by permanent cell cycle arrest, has been extensively studied in mitotic cells such as fibroblasts. However, senescent cells have also been observed in the brain. Even though it is recognized that cellular energetic metabolism and redox homeostasis are perturbed in the aged brain and neurodegenerative diseases (NDDs), it is still unknown which alterations in the overall physiology can stimulate cellular senescence induction and their relationship with the former events. Recent Advances: Recent findings have shown that during prolonged inflammatory and pathologic events, the blood-brain barrier could be compromised and immune cells might enter the brain; this fact along with the brain's high oxygen dependence might result in oxidative damage to macromolecules and therefore senescence induction. Thus, cellular senescence in different brain cell types is revised here. Critical Issues: Most information related to cellular senescence in the brain has been obtained from research in glial cells since it has been assumed that the senescent phenotype is a feature exclusive to mitotic cells. Nevertheless, neurons with senescence hallmarks have been observed in old mouse brains. Therefore, although this is a controversial topic in the field, here we summarize and integrate the observations from several studies and propose that neurons indeed senesce. Future Directions: It is still unknown which alterations in the overall metabolism can stimulate senescence induction in the aged brain, what are the mechanisms and signaling pathways, and what is their relationship to NDD development. The understanding of these processes will expose new targets to intervene age-associated pathologies.

Filiaciones:
Angel Maciel-Baron, Luis:
 Univ Autonoma Metropolitana Iztapalapa, Dept Ciencias Salud, Div Ciencias Biol & Salud, Av San Rafael Altixco 186,AP 55-535, Iztapalapa 09340, Mexico

 UAMI, Biol Expt, Iztapalapa, Mexico

Moreno-Blas, Daniel:
 Univ Nacl Autonoma Mexico, Inst Fisiol Celular, Dept Neurodesarrollo & Fisiol, Ciudad De Mexico, Mexico

 UNAM, Ciencias Bioquim, Ciudad De Mexico, Mexico

Lizbeth Morales-Rosales, Sandra:
 Univ Autonoma Metropolitana Iztapalapa, Dept Ciencias Salud, Div Ciencias Biol & Salud, Av San Rafael Altixco 186,AP 55-535, Iztapalapa 09340, Mexico

 UAMI, Biol Expt, Iztapalapa, Mexico

Yazmin Gonzalez-Puertos, Viridiana:
 Univ Autonoma Metropolitana Iztapalapa, Dept Ciencias Salud, Div Ciencias Biol & Salud, Av San Rafael Altixco 186,AP 55-535, Iztapalapa 09340, Mexico

Edith Lopez-Diazguerrero, Norma:
 Univ Autonoma Metropolitana Iztapalapa, Dept Ciencias Salud, Div Ciencias Biol & Salud, Av San Rafael Altixco 186,AP 55-535, Iztapalapa 09340, Mexico

Torres, Claudio:
 Drexel Univ, Coll Med, Dept Pathol & Lab Med, Philadelphia, PA 19104 USA

Castro-Obregon, Susana:
 Univ Nacl Autonoma Mexico, Inst Fisiol Celular, Dept Neurodesarrollo & Fisiol, Ciudad De Mexico, Mexico

Konigsberg, Mina:
 Univ Autonoma Metropolitana Iztapalapa, Dept Ciencias Salud, Div Ciencias Biol & Salud, Av San Rafael Altixco 186,AP 55-535, Iztapalapa 09340, Mexico
ISSN: 15230864
Editorial
MARY ANN LIEBERT INC, 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA, Estados Unidos America
Tipo de documento: Review
Volumen: 28 Número: 18
Páginas: 1704-1723
WOS Id: 000432860900007
ID de PubMed: 28467755

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