Mechanisms of Glia and Non-coding RNAs in Traumatic Brain Injury:Insights and Intervention Strategies

Traumatic brain injury (TBI) is a globally prevalent neurological disorder, with longterm deteriorating neurological deficits (especially learning and memory impairments). Classified into primary and secondary injuries, TBI’s secondary phase is characterized by inflammation and apoptosis—key pathological processes driving further neurological dysfunction with complex bidirectional regulation. This study systematically elaborates the core mechanisms: glial cells act as central "regulatory hubs" that modulate their phenotype via proinflammatory factor release and key signaling pathway activation, directly or indirectly inducing neuronal apoptosis; non-coding RNAs [Long Non-coding RNAs (lncRNAs), MicroRNAs (miRNAs)] function as "molecular bridges" by targeting glial activation, inflammatory factor secretion, and apoptosis-related pathways [e.g., LINC00707/miR-30a-5p, miR-21-5p/ phosphatase and tensin homologue (PTEN)]. Additionally, diverse therapeutic strategies are summarized: pharmacological agents (e.g., minocycline, dexmedetomidine) inhibit inflammatory pathways and reduce apoptosis-related proteins; mesenchymal stem cell therapy exerts immunomodulatory and neuroregenerative effects; nanoparticles enable precise drug delivery; hyperbaric oxygen therapy blocks the vicious cycle by improving oxygenation; gut microbiota interventions restore homeostasis via metabolic and immune modulation. In conclusion, in-depth analysis of glial cells and non-coding RNAs in TBI-induced inflammation and apoptosis provides a theoretical basis for developing targeted therapies, holding great significance for improving TBI patient prognosis.