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<p>Diabetic cardiomyopathy (DCM) is a prevalent diabetes-related cardiac complication. miR-671-5p has been shown to mitigate ischemia-reperfusion-induced cardiomyocyte injury. This study investigated the role and underlying mechanisms of miR-671-5p in a DCM cell model established by exposing AC16 cardiomyocytes to high glucose (HG). The miRNA expression dataset GSE210036 from diabetic mouse hearts was analyzed. Cell injury was evaluated by assessing cell viability, apoptosis, and ferroptosis-related alterations. The expression levels and interactions of miR-671-5p, circHUWE1, and CELF1 were examined in the cell model. p38 MAPK activation was further assessed following modulation of the circHUWE1/miR-671-5p/CELF1 axis. Additionally, the m6A modification of circHUWE1 was evaluated. Bioinformatics analysis revealed decreased miR-671-5p expression in diabetic mouse hearts compared to healthy controls. HG treatment downregulated miR-671-5p expression and upregulated the levels of circHUWE1 and CELF1. circHUWE1 upregulation resulted from diminished METTL3-dependent m6A modification. Both miR-671-5p mimic and circHUWE1 knockdown attenuated HG-induced apoptosis and ferroptosis-related alterations. Mechanistically, circHUWE1 elevated CELF1 expression and subsequently activated p38 MAPK by sponging miR-671-5p. The cardioprotective effects of dexmedetomidine (Dex) are associated with the circHUWE1/miR-671-5p/CELF1 axis. In conclusion, the circHUWE1/miR-671-5p/CELF1 axis regulates HG-induced cardiomyocyte apoptosis and ferroptosis-related alterations and represents a novel mechanism underlying Dex-mediated cardioprotection.</p>

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METTL3-mediated N6-methyladenosine modification of circHUWE1 promotes high glucose-induced cardiomyocyte apoptosis and ferroptosis-related alterations through regulating miR-671-5p/CELF1 axis

  • 期刊论文

  • 发表日期：

    2026年7月16日

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  • Ye Yu,
  • Zihan Ma,
  • Lei Shi,
  • Li Ding

摘要

Diabetic cardiomyopathy (DCM) is a prevalent diabetes-related cardiac complication. miR-671-5p has been shown to mitigate ischemia-reperfusion-induced cardiomyocyte injury. This study investigated the role and underlying mechanisms of miR-671-5p in a DCM cell model established by exposing AC16 cardiomyocytes to high glucose (HG). The miRNA expression dataset GSE210036 from diabetic mouse hearts was analyzed. Cell injury was evaluated by assessing cell viability, apoptosis, and ferroptosis-related alterations. The expression levels and interactions of miR-671-5p, circHUWE1, and CELF1 were examined in the cell model. p38 MAPK activation was further assessed following modulation of the circHUWE1/miR-671-5p/CELF1 axis. Additionally, the m6A modification of circHUWE1 was evaluated. Bioinformatics analysis revealed decreased miR-671-5p expression in diabetic mouse hearts compared to healthy controls. HG treatment downregulated miR-671-5p expression and upregulated the levels of circHUWE1 and CELF1. circHUWE1 upregulation resulted from diminished METTL3-dependent m6A modification. Both miR-671-5p mimic and circHUWE1 knockdown attenuated HG-induced apoptosis and ferroptosis-related alterations. Mechanistically, circHUWE1 elevated CELF1 expression and subsequently activated p38 MAPK by sponging miR-671-5p. The cardioprotective effects of dexmedetomidine (Dex) are associated with the circHUWE1/miR-671-5p/CELF1 axis. In conclusion, the circHUWE1/miR-671-5p/CELF1 axis regulates HG-induced cardiomyocyte apoptosis and ferroptosis-related alterations and represents a novel mechanism underlying Dex-mediated cardioprotection.