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<p>This study aimed to investigate the role of mitophagy mediated by the hypoxia-inducible factor-1α (HIF-1α)/Bcl-2/adenovirus E1B 19-kDa interacting protein (BNIP3) pathway in mitigating renal injury induced by intermittent hypoxia (IH), a hallmark of obstructive sleep apnea (OSA).&#xa0;Human renal tubular epithelial cells (RTECs) were exposed to IH conditions using a hypoxia-reoxygenation chamber for 24&#xa0;h. Cells were divided into five groups: normoxia, IH, IH with HIF-1α siRNA (IH + si-HIF-1α), IH with BNIP3 siRNA (IH + siBNIP3), and IH with HIF-1α siRNA plus BNIP3 overexpression (IH + si-HIF-1α + BNIP3). Cell viability, apoptosis, mitochondrial morphology, and mitophagy levels were assessed using flow cytometry, western blotting, transmission electron microscopy, and immunofluorescence.&#xa0;Under IH conditions, inhibition of HIF-1α or BNIP3 significantly reduced cell viability, increased apoptosis, disrupted mitochondrial structure, and decreased mitophagy levels in RTECs. Overexpression of BNIP3 in the presence of HIF-1α inhibition restored mitophagy levels, attenuated cellular damage and apoptosis, and improved mitochondrial morphology.&#xa0;These findings demonstrate that mitophagy mediated by the HIF-1α/BNIP3 signaling pathway plays a protective role in IH-induced renal injury, suggesting that targeted enhancement of mitophagy may provide a potential therapeutic strategy for OSA-related kidney dysfunction.</p>

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Mitophagy protects renal tubular epithelial cells from intermittent hypoxia-induced injury via the HIF-1α/BNIP3 pathway

  • 期刊论文

  • 发表日期：

    2025年12月15日

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  • Xiao-Bin Zhang,
  • Qi-Feng Gan,
  • Yu-Xin Guo,
  • Li-Da Chen,
  • Li-Qin Zhang,
  • Ling Cai,
  • Ya-Ting Yuan,
  • Jing-Huang Cai,
  • Xiang-Xin Chen

摘要

This study aimed to investigate the role of mitophagy mediated by the hypoxia-inducible factor-1α (HIF-1α)/Bcl-2/adenovirus E1B 19-kDa interacting protein (BNIP3) pathway in mitigating renal injury induced by intermittent hypoxia (IH), a hallmark of obstructive sleep apnea (OSA). Human renal tubular epithelial cells (RTECs) were exposed to IH conditions using a hypoxia-reoxygenation chamber for 24 h. Cells were divided into five groups: normoxia, IH, IH with HIF-1α siRNA (IH + si-HIF-1α), IH with BNIP3 siRNA (IH + siBNIP3), and IH with HIF-1α siRNA plus BNIP3 overexpression (IH + si-HIF-1α + BNIP3). Cell viability, apoptosis, mitochondrial morphology, and mitophagy levels were assessed using flow cytometry, western blotting, transmission electron microscopy, and immunofluorescence. Under IH conditions, inhibition of HIF-1α or BNIP3 significantly reduced cell viability, increased apoptosis, disrupted mitochondrial structure, and decreased mitophagy levels in RTECs. Overexpression of BNIP3 in the presence of HIF-1α inhibition restored mitophagy levels, attenuated cellular damage and apoptosis, and improved mitochondrial morphology. These findings demonstrate that mitophagy mediated by the HIF-1α/BNIP3 signaling pathway plays a protective role in IH-induced renal injury, suggesting that targeted enhancement of mitophagy may provide a potential therapeutic strategy for OSA-related kidney dysfunction.