Published online Jul 26, 2025. doi: 10.4252/wjsc.v17.i7.101929
Revised: March 7, 2025
Accepted: June 25, 2025
Published online: July 26, 2025
Processing time: 162 Days and 1.2 Hours
Spinal cord injury (SCI) often results in irreversible neurological deficits; there
To explore the role of XIST in enhancing NSC function and its therapeutic po
We used in vitro and in vivo models to examine the effects of XIST on NSCs. XIST was overexpressed in NSCs, and its impact on mitochondrial function, neuronal differentiation, and the insulin-like growth factor 2 mRNA binding protein 2 (IGF2BP2)/carnitine palmitoyl transferase 1A (CPT1A) pathway was assessed using a series of biochemical assays, quantitative PCR, and Seahorse XF24 ana
Overexpression of XIST in NSCs significantly increased mitochondrial membrane potential, ATP production, and oxygen consumption rate. XIST also promoted NSC proliferation and neuronal differentiation while inhibiting astrocytic differentiation. Mechanistically, XIST regulated CPT1A expression post-transcriptionally by interacting with IGF2BP2. In vivo XIST-treated mice exhibited im
These findings suggested that XIST modulated mitochondrial function and neural differentiation in NSCs through the IGF2BP2/CPT1A pathway. While preliminary in vivo results are encouraging, further studies are needed to determine the long-term therapeutic relevance and underlying mechanisms of XIST in SCI recovery.
Core Tip: This study highlighted the critical role of long non-coding RNA X inactive-specific transcript (XIST) in enhancing neural stem cell function for spinal cord injury (SCI) treatment. XIST significantly improved motor recovery and reduced inflammation in mouse models of SCI by promoting mitochondrial function and neuronal differentiation. These findings suggested that XIST regulated carnitine palmitoyl transferase 1A expression via the insulin-like growth factor 2 mRNA binding protein 2 pathway, providing a promising therapeutic target for the development of effective interventions against irreversible neurological deficits in SCI. Further exploration of the long-term effects of XIST may advance its clinical applications.