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Peer-reviewedCC BYFrontiers in molecular neuroscience

Mitochondrial metabolic remodeling and blood–brain barrier dysfunction after repetitive mild traumatic brain injury

  • Lingjuan Gao1
  • Xincheng Xue1
  • Xianhui Deng2
  • Yu Xu1
  • Heng Gao1
  1. 1Department of Neurosurgery, Jiangyin Clinical College of Xuzhou Medical University , , ,
  2. 2Department of Neonatology, Jiangyin People’s Hospital , , ,
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Abstract

Repetitive mild traumatic brain injury (rmTBI) may arise when concussive or subconcussive impacts recur before physiological recovery is complete. Mitochondrial dysfunction and blood–brain barrier (BBB) impairment are shared features across the traumatic brain injury (TBI) spectrum; in rmTBI, repetition may alter their magnitude, duration, and temporal coupling. This focused narrative review evaluates evidence that mitochondrial metabolic remodeling contributes to neurovascular-unit dysfunction after rmTBI. We discuss energy failure, mitochondrial reactive oxygen species, succinate, fumarate, alpha-ketoglutarate, NAD + depletion, and lactate as candidate links between metabolic stress and BBB injury. Direct rmTBI evidence is prioritized, while single-TBI studies are used as mechanistic context when rmTBI data are limited. Available studies support a model in which recurrent metabolic stress, redox imbalance, inflammatory signaling, and impaired mitochondrial quality control converge on endothelial and multicellular neurovascular-unit dysfunction. Metabolism-directed interventions are promising but require validation across rigorously defined rmTBI paradigms and clinical cohorts.

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Cite

BibTeXRIS
BibTeX
@article{gao2026mitochondrial,
  title = {{Mitochondrial metabolic remodeling and blood–brain barrier dysfunction after repetitive mild traumatic brain injury}},
  author = {Lingjuan Gao and Xincheng Xue and Xianhui Deng and Yu Xu and Heng Gao},
  journal = {Frontiers in molecular neuroscience},
  year = {2026},
  month = oct,
  doi = {10.3389/fnmol.2026.1852115},
  url = {https://europepmc.org/article/PMC/PMC13720597},
  note = {CC BY},
}
RIS
TY  - JOUR
TI  - Mitochondrial metabolic remodeling and blood–brain barrier dysfunction after repetitive mild traumatic brain injury
AU  - Lingjuan Gao
AU  - Xincheng Xue
AU  - Xianhui Deng
AU  - Yu Xu
AU  - Heng Gao
PY  - 2026
DA  - 2026/10/16
JO  - Frontiers in molecular neuroscience
DO  - 10.3389/fnmol.2026.1852115
UR  - https://europepmc.org/article/PMC/PMC13720597
AB  - Repetitive mild traumatic brain injury (rmTBI) may arise when concussive or subconcussive impacts recur before physiological recovery is complete. Mitochondrial dysfunction and blood–brain barrier (BBB) impairment are shared features across the traumatic brain injury (TBI) spectrum; in rmTBI, repetition may alter their magnitude, duration, and temporal coupling. This focused narrative review evaluates evidence that mitochondrial metabolic remodeling contributes to neurovascular-unit dysfunction after rmTBI. We discuss energy failure, mitochondrial reactive oxygen species, succinate, fumarate, alpha-ketoglutarate, NAD + depletion, and lactate as candidate links between metabolic stress and BBB injury. Direct rmTBI evidence is prioritized, while single-TBI studies are used as mechanistic context when rmTBI data are limited. Available studies support a model in which recurrent metabolic stress, redox imbalance, inflammatory signaling, and impaired mitochondrial quality control converge on endothelial and multicellular neurovascular-unit dysfunction. Metabolism-directed interventions are promising but require validation across rigorously defined rmTBI paradigms and clinical cohorts.
SN  - 1662-5099
ER  -