Emerging evidence suggests that neuroinflammation is an underlying cause of aging, neurodegeneration, and traumatic injury in the central nervous system (CNS) [1]. Anti-inflammatory treatment modalities therefore hold great promise in these pathological conditions. CISD2 (CDGSH iron sulfur domain 2), as an outer mitochondrial membrane protein, is beneficial against cellular apoptosis by maintaining mitochondrial integrity and thereby preventing mitochondrial dysfunction [2]. We previously found that CISD2 deficiency exacerbated mitochondrial dysfunction and augmented inflammatory cascades associated with aging, CNS disease or injury [1].
from Journal of the Neurological Sciences https://ift.tt/32PChrn
from Journal of the Neurological Sciences https://ift.tt/32PChrn
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