ArticleNeurotrauma reports
Effects of GLP-1 Receptor Agonist Exenatide on Mitochondrial Dysfunction After Spinal Cord Injury.
Article in Neurotrauma reports. 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
6 authors.
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Abstract
Spinal cord injury (SCI) triggers secondary pathological processes, including inflammation, oxidative stress, and mitochondrial dysfunction, that contribute to progressive neuronal damage. Because mitochondria play a central role in cellular homeostasis, mitochondrial impairment is considered an important component of SCI pathophysiology. We investigated the effects of exenatide, a glucagon-like peptide-1 (GLP-1) receptor agonist, on mitochondrial dysfunction after SCI using a rat contusion model and C6 glioma cells. Exenatide was associated with increased OPA1 expression and enhanced Drp1 phosphorylation at Ser637, suggesting a shift in mitochondrial dynamics toward fusion-dominant regulation. Exenatide also tended to increase the expression of Bcl-2, HO-1, and p62.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.