ReviewCancer gene therapy2026
Blood-brain barrier breakdown in traumatic brain injury: current insights and future directions.
Review in Cancer gene therapy, 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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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Authors and funding
9 authors.
Funding
Abstract
Traumatic brain injury (TBI) is among the most devastating condition and involves primary and secondary injury cascades. The blood-brain barrier (BBB) is a selective, semipermeable membrane that tightly controls the brain's microenvironment for proper neuronal function. Existing evidence demonstrates that TBI impairs the integrity and function of the BBB, leading to not only acute pathological changes but also long-term neuropathological consequences. Multiple BBB-related signaling molecules (e.g., Tie-2, EphB3, and Cav-1) are involved in the pathophysiological processes post-injury. These can result in microcirculatory insufficiency, neurotoxin accumulation, and cerebral edema after TBI. Together, such events synergistically cause axonal damage, neuronal cell death, and neuroinflammatory responses, which underlie the pathogenesis of TBI. In this review, we aim to summarize the pathophysiological roles of BBB breakdown in TBI, survey underlying mechanisms, and discuss therapeutic potential for this notorious disease by regulating the BBB.
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Registered trials
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