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May 15, 20260 citations

The Role of hsacirc₀076767 in Mitochondrial Injury During Myocardial Ischemia/Reperfusion: a Focus on miR-140-3p and the Hypoxia-Inducible Factor-1α/β-Catenin Pathway.

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RXRuibing XieSXShuYun XiaXCXiaoFang Chen

Key Points

  • This research aimed to assess the role of hsa_circ_0076767 in worsening mitochondrial injury during myocardial ischemia/reperfusion by targeting miR-140-3p.
  • Established MI/RI and hypoxia/reoxygenation cell models.
  • Utilized RT-qPCR, flow cytometry, and various staining techniques to evaluate mitochondrial and cardiac tissue injury.
  • Conducted dual-luciferase and RNA pull-down assays to examine interactions between hsa_circ_0076767 and miR-140-3p.
  • hsa_circ_0076767 was upregulated in MI/RI mice and hypoxia/reoxygenation cell models.
  • Silencing hsa_circ_0076767 reduced myocardial tissue injury and mitochondrial damage.
  • hsa_circ_0076767 was found to target miR-140-3p and inhibit the HIF-1α/β-catenin pathway.

Abstract

OBJECTIVE: This study aimed to investigate whether hsacirc₀076767 exacerbates mitochondrial injury during myocardial ischemia/reperfusion injury (MI/RI) by targeting miR-140-3p and directly inhibiting the hypoxia-inducible factor (HIF) -1α/β-catenin pathway. METHODS: MI/RI and hypoxia/reoxygenation (H/R) cell models were established. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was performed to determine hsacirc₀076767 expression in both the MI/RI models and to detect the subcellular localization of hsacirc₀076767 and its responsiveness to ribonuclease R in HL-1 cells. A loss-of-function assay was performed to examine the function of hsacirc₀076767 in cardiomyocyte mitochondrial and cardiac tissue injury following MI/RI. Hematoxylin-eosin staining and terminal deoxynucleotidyl transferase dUTP nick end labeling staining were used to assess myocardial tissue injury and apoptosis of myocardial tissues in mice, respectively. hsacirc₀076767 was assayed for cell viability using Cell Counting Kit-8, for apoptosis using flow cytometry, for mitochondrial membrane potential using JC-1, and for cellular adenosine triphosphate content using commercial kits. RT-qPCR and protein blotting were performed to detect gene expression. Dual-luciferase, ribonucleic acid pull-down, and fluorescence in situ hybridization co-localization assays were used to validate the interaction between hsacirc₀076767 and miR-140-3p. Finally, the regulatory relationship between hsacirc₀076767 and the HIF-1α/β-catenin pathway was verified. RESULTS: hsacirc₀076767 was upregulated in myocardial tissues of MI/RI mice and H/R HL-1 cells. Silencing hsacirc₀07676767 ameliorated myocardial tissue injury, apoptosis, and mitochondrial damage in cardiomyocytes. hsacirc₀076767 targets miR-140-3p. Moreover, hsacirc₀076767 promoted mitochondrial injury by inhibiting the HIF-1α/β-catenin pathway. CONCLUSION: hsacirc₀076767 targets miR-140-3p and directly inhibits the HIF-1α/β-catenin pathway, exacerbating mitochondrial damage in cardiomyocytes during MI/RI.

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Cite This Study

Xie et al. (2026) studied this question.

synapsesocial.com/papers/6a06b888e7dec685947ab0b2https://doi.org/10.21470/1678-9741-2024-0451
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