ReviewCellular and molecular neurobiology2026
The AMPK-BECN1-System Xc⁻ Pathway in Traumatic Brain Injury: Implications for Exosome-Based Therapy.
Review in Cellular and molecular neurobiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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6 authors.
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Abstract
Secondary neuronal death following traumatic brain injury (TBI) constitutes a central pathological mechanism driving permanent functional deficits. Mounting evidence reveals the “autophagy-ferroptosis axis,” forged by dysfunctional autophagy converging with activated ferroptosis, as a critical driver of this process. This review synthesizes current evidence on the molecular underpinnings of this axis within TBI, suggesting the AMPK (AMP-activated protein kinase)-BECN1 (beclin 1)-System Xc⁻ pathway as one potential core regulatory network. We provide an in-depth exploration of how this network may orchestrate neuronal fate through the “upstream decision-making” of the energy sensor AMPK, the “dual-function bridge” role of BECN1, and the “terminal executioner” function of System Xc⁻. Building upon this foundation, the review further advances an intervention hypothesis leveraging exosomes derived from olfactory ensheathing cells overexpressing brain-derived neurotrophic factor (BDNF-OE-OEC-Exos). We suggest their potential for TBI therapy, while acknowledging that this concept remains to be validated in relevant disease models and human studies.
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