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Cell Death Dis ; 14(8): 496, 2023 08 03.
Artigo em Inglês | MEDLINE | ID: mdl-37537168

RESUMO

Traumatic Brain injury-induced disturbances in mitochondrial fission-and-fusion dynamics have been linked to the onset and propagation of neuroinflammation and neurodegeneration. However, cell-type-specific contributions and crosstalk between neurons, microglia, and astrocytes in mitochondria-driven neurodegeneration after brain injury remain undefined. We developed a human three-dimensional in vitro triculture tissue model of a contusion injury composed of neurons, microglia, and astrocytes and examined the contributions of mitochondrial dysregulation to neuroinflammation and progression of injury-induced neurodegeneration. Pharmacological studies presented here suggest that fragmented mitochondria released by microglia are a key contributor to secondary neuronal damage progression after contusion injury, a pathway that requires astrocyte-microglia crosstalk. Controlling mitochondrial dysfunction thus offers an exciting option for developing therapies for TBI patients.


Assuntos
Lesões Encefálicas Traumáticas , Contusões , Humanos , Doenças Neuroinflamatórias , Inflamação/metabolismo , Encéfalo/metabolismo , Lesões Encefálicas Traumáticas/metabolismo , Contusões/metabolismo , Mitocôndrias/metabolismo , Microglia/metabolismo , Astrócitos/metabolismo
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