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Cellular Senescence, Neurological Function, and Redox State
Journal article   Peer reviewed

Cellular Senescence, Neurological Function, and Redox State

Luis Ángel Maciel-Barón, Daniel Moreno-Blas, Sandra Lizbeth Morales-Rosales, Viridiana Yazmín González-Puertos, Norma Edith López-Díazguerrero, Claudio Torres, Susana Castro-Obregón and Mina Königsberg
Antioxidants & redox signaling, v 28(18), pp 174-1723
20 Jun 2018
PMID: 28467755

Abstract

Forum Review Articles
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.— Antioxid. Redox Signal. 28, 1704–1723.

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Domestic collaboration
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Web of Science research areas
Biochemistry & Molecular Biology
Endocrinology & Metabolism
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