REVIEW article
Front. Cell. Neurosci.
Sec. Cellular Neuropathology
This article is part of the Research TopicIntercellular communication in chronic neuroinflammatory diseasesView all 7 articles
Neural stem cells fate under neuroinflammatory conditions and oxidative stress response
Provisionally accepted
- 1Department of Drug and Health Sciences, University of Catania, 95123 Catania, Italy, Catania, Italy
- 2Department of Biomedical and Biotechnological Sciences, University of Catania, 95123 Catania Italy, Catania, Italy
- 3Department of Medicine and Surgery, University of Enna “Kore”, 94100 Enna, Italy, Enna, Italy
Select one of your emails
You have multiple emails registered with Frontiers:
Notify me on publication
Please enter your email address:
If you already have an account, please login
You don't have a Frontiers account ? You can register here
Neural stem cells (NSCs) are defined by their self-renewal capacity and multipotent differentiation potential, making them essential for nervous system development and for the maintenance of adult brain homeostasis. Although confined to the subventricular zone and the subgranular zone of the hippocampus in adulthood, NSCs preserve a functional capacity for neurogenesis and tissue regeneration. This regenerative potential becomes particularly important in neuropathological conditions, where tissue damage is often accompanied by neuroinflammation and oxidative stress. Within this hostile microenvironment, NSCs have to cope with inflammatory mediators and reactive oxygen species that can affect their survival, proliferation, and cellular differentiation. NSCs also are actively modulated by diverse molecular pathways in response to stress conditions promoting stemness or stem cell exhaustion. Therefore, understanding the crosstalk between neuroinflammatory and oxidative stress in NSCs fate is crucial for elucidating the mechanisms of neurogenesis and homeostasis recovery and for designing therapeutic strategies.
Keywords: Cytokines, differentiation, Metabolic rewiring, Nrf2, redox homeostasis
Received: 31 Oct 2025; Accepted: 03 Dec 2025.
Copyright: © 2025 Torrisi, Denaro, Ragonese, D'Aprile, Zappala' and Parenti. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence:
Filippo Torrisi
Rosalba Parenti
Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.