Sirtuin1 in Spinal Cord Injury: Regulatory Mechanisms, Microenvironment Remodeling and Therapeutic Potential

CNS Neuroscience & Therapeutics, Journal Year: 2025, Volume and Issue: 31(2)

Published: Feb. 1, 2025

ABSTRACT Background Spinal cord injury (SCI) is a complex central nervous system disorder characterized by multifaceted pathological processes, including inflammation, oxidative stress, programmed cell death, autophagy, and mitochondrial dysfunction. Sirtuin 1 (Sirt1), critical NAD + ‐dependent deacetylase, has emerged as promising therapeutic target for SCI repair due to its potential protect neurons, regulate glial vascular cells, optimize the microenvironment. However, regulatory roles of Sirt1 in are challenging, effects vary depending on activation timing, expression levels, types. Methods A systematic literature review was conducted using PubMed, Scopus, Web Science identify studies investigating SCI. Relevant publications were analyzed synthesize current evidence Sirt1's mechanisms, effects, challenges repair. Results exerts broad across diverse processes types post‐SCI. It promotes neuronal survival axonal regeneration, modulates astrocytes microglia resolve supports oligodendrocyte‐mediated myelination, enhances endothelial function. Proper may mitigate secondary injury, whereas excessive or prolonged could impair inflammatory resolution disrupt cellular homeostasis. This highlights therapies, but include optimizing spatiotemporal addressing dual different Conclusion Targeting represents viable strategy repair, given regulation neuroprotection, immunomodulation, tissue remodeling. translating these findings into therapies requires resolving issues such type‐specific delivery, precise dosage control. provides theoretical foundation practical insights advancing Sirt1‐based treatments

Language: Английский

Quercetin inhibits oligodendrocytes ferroptosis by blocking NCOA4-mediated ferritinophagy

International Immunopharmacology, Journal Year: 2025, Volume and Issue: 150, P. 114152 - 114152

Published: Feb. 12, 2025

Language: Английский