ArticleCell death discovery2025
Effects of astrocytic PKM2 gene deletion on neuronal death following traumatic brain injury.
Article in Cell death discovery, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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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Who cites it
1 citing paper in PubMed.
- Roles of lactate and protein lactylation in neurogenesis and neurodegenerative disease.Journal of translational medicine · 2026Review
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Authors and funding
10 authors.
Funding
Abstract
Traumatic brain injury (TBI) is a critical condition caused by physical trauma to the head, leading to primary brain edema, hemorrhage, and swelling, along with secondary injuries such as oxidative damage, neuroinflammation, and mitochondrial dysfunction. Astrocytes play a vital role in the astrocyte-neuron lactate shuttle (ANLS), which facilitates the transfer of lactate from astrocytes to neurons as an energy source. This study investigates the role of the pyruvate kinase M2 (PKM2) gene in astrocytes and its impact on neuronal survival following TBI. We hypothesized that deletion of the PKM2 gene in astrocytes would result in increased neuronal death due to impaired lactate supply via the ANLS. Additionally, we hypothesized that lactate administration post-TBI would mitigate neuronal death and alleviate cognitive impairment. To test these hypotheses, we utilized tamoxifen to specifically delete the PKM2 gene in astrocytes of Aldh1l1-Cre
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