ArticleCNS neuroscience & therapeutics2025
ARIP1 Deficiency Facilitates the Inhibition of Neuronal Ferroptosis in Cerebral Ischemia by Activin A Through SMAD3 and p38 MAPK Signaling.
Article in CNS neuroscience & therapeutics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- M2 Macrophage-Derived Exosomes Ameliorate BPD by Inhibiting Ferroptosis via Suppression of the ZAKα-p38 Signaling Pathway.Antioxidants (Basel, Switzerland) · 2026Article
- ARIP1 Deficiency Facilitates the Inhibition of Neuronal Ferroptosis in Cerebral Ischemia by Activin A Through SMAD3 and p38 MAPK Signaling.CNS neuroscience & therapeutics · 2025Article
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Authors and funding
8 authors.
Funding
Abstract
introductionFerroptosis is an essential pathophysiological process in cerebral ischemic injury. Activin receptor-interacting protein 1 (ARIP1) is a negative regulator of the activin signaling pathway in neurons.
objectiveThis study investigated whether activin A inhibits neuronal ferroptosis and the role of ARIP1 in cerebral ischemic injury. METHODS AND
resultsIn this study, activin A increased the viability of primary neurons under conditions of oxygen-glucose deprivation (OGD). Subsequent RNA-sequencing analysis of activin A-treated neurons identified expression of Slc7a11 as the ferroptosis-associated gene with significant upregulation. Next, using the CRISPR/Cas9 system, mice were generated with a heterozygous deficiency of ARIP1 (Arip1
conclusionThese findings indicate that downregulating the expression of ARIP1 suppresses neuronal ferroptosis by modulating SLC7A11/GPX4 expression via SMAD3 and p38 MAPK signaling, ultimately enhancing the neuroprotective role of activin A against cerebral ischemia.
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