ArticleMolecular neurobiology2026
SIRT3/AARS2 regulates SOD2 lactylation to determine neuronal fate in TBI.
Article in 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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Abstract
Lactate accumulation is strongly associated with poor neurological outcomes in traumatic brain injury (TBI), creating a "lactate paradox" given its role as an energy substrate in the early stages of trauma. Imbalanced reactive oxygen species (ROS) act as cell injury factors throughout the pathological progression of TBI. This study aims to elucidate the key mechanisms connecting dysregulated lactate metabolism and cellular damage. We discovered that the high-lactate environment induced by TBI drives lysine lactylation of the mitochondrial antioxidant enzyme superoxide dismutase 2 (SOD2), inhibiting its enzymatic activity and leading to mitochondrial ROS (mtROS) accumulation. Mechanistically, aminoacyl-tRNA synthetase 2 (AARS2) and NAD
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