ArticleTranslational neuroscience2026
Regulation of FTO on PDCD5 mRNA stability to mediate neuron apoptosis in rats with hypoxic-ischemic brain damage.
Article in Translational neuroscience, 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
Objectives: This study explored the mechanism of FTO in regulating neuron apoptosis in hypoxic-ischemic brain damage (HIBD) models via PDCD5. Methods: Neonatal SD rats were treated by unilateral common carotid artery ligation to establish HIBD model, while primary hippocampal neurons were induced by oxygen-glucose deprivation (OGD) to mimic the Results: HIBD rats had decreased FTO expression and elevated PDCD5 expression, accompanied by increased cerebral infarction and apoptosis. Overexpression of FTO inhibited neuronal apoptosis and alleviated HIBD progression. Additionally, knockdown of PDCD5 suppressed OGD-induced neuronal apoptosis in OGD-induced primary hippocampal neurons, while such effect was nullified by overexpression of FTO. FTO interacted with PDCD5 to influence the m6A modification level of PTBP1 and subsequently decrease its mRNA stability. Conclusions: Down-regulation of FTO expression in HIBD reduces the degradation of M6A-modified PDCD5 mRNA, thereby increasing PDCD5 protein expression. This elevation in PDCD5 promotes neuronal apoptosis, which exacerbates the progression of HIBD.
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