ArticleMolecular neurobiology2025
miR-758-3p Interferes with Neuronal Apoptosis in Cerebral Ischemia-Reperfusion by Inhibiting ILK.
Article in Molecular neurobiology, 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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Who cites it
1 citing paper in PubMed.
- Mechanism of Astragaloside IV Against Cerebral Ischemia-Reperfusion Injury: Inhibiting Neuronal Apoptosis via the CytC/Apaf-1 Mitochondrial Pathway.Pharmaceuticals (Basel, Switzerland) · 2026Article
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Authors and funding
13 authors.
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Abstract
This study investigated the role of integrin-linked kinase (ILK) in neuronal apoptosis induced by cerebral ischemia‒reperfusion injury (CIRI) and its interaction with a circRNA (0000964) and miR-758-3p. Using in vivo and in vitro rat models, we clarified how ILK regulates neuronal apoptosis during CIRI. Our findings revealed that ILK expression is upregulated in response to CIRI and is modulated by the circRNA (0000964)/miR-758-3p axis. This study provides new insights into the molecular mechanisms of CIRI and suggests potential therapeutic targets to reduce neuronal apoptosis. A CIRI rat model was created through middle cerebral artery occlusion (MCAO). After miR-758-3p overexpression, neurological deficits, CIRI volume, and the expression levels of circRNAs (0000964) and ILK were evaluated. Neurons were subjected to oxygen‒glucose deprivation (OGD) to simulate in vitro CIRI, and the same molecules were analyzed. MCAO-induced CIRI downregulated a circRNA (0000964) and upregulated ILK and miR-758-3p. Similarly, in vitro OGD-induced apoptosis downregulated a circRNA (0000964) and upregulated ILK and miR-758-3p. Further analysis confirmed that a circRNA (0000964) negatively regulates miR-758-3p, which in turn negatively regulates ILK. This axis controls ILK and Caspase-3 expression, influencing neuronal apoptosis. ILK has been identified as a key regulator of neuronal apoptosis in CIRI. The circRNA (0000964)/miR-758-3p axis modulates ILK, impacting neuronal survival. This molecular network offers new insights into CIRI pathophysiology and highlights possible therapeutic approaches.
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Registered trials
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