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<p>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.</p>

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miR-758-3p Interferes with Neuronal Apoptosis in Cerebral Ischemia–Reperfusion by Inhibiting ILK

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年2月12日

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  • Xiaoli Min,
  • Xuesong Bai,
  • Qing Zhao,
  • Wenwu Yang,
  • Sixian Lin,
  • Lei Xian,
  • Rui Jing,
  • Xuhui Li,
  • Wenji Jia,
  • Wei Miao,
  • Mei Yin,
  • Feifei Shang,
  • Yong Zeng

摘要

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.