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<p>Lung development is a highly programmed and energy-dependent dynamic process, with the fetal and neonatal periods representing critical developmental windows. Emerging evidence indicates that mitochondrial quality control (MQC) mechanisms—including mitophagy, mitochondrial dynamics (fusion/fission), and mitochondrial biogenesis—play a central regulatory role in pulmonary development and injury responses during these periods. While, under stressors in the maternal-fetal environment or hyperoxia therapy, transiently upregulate MQC may serve as protective compensatory response, MQC dysregulation can lead to the accumulation of dysfunctional mitochondria, exacerbated oxidative stress, aberrant cellular metabolism, and amplified inflammatory responses. These disruptions contribute to pathological sequelae such as impaired alveolar epithelial differentiation, aberrant pulmonary vascular remodeling, diminished antioxidant capacity, and failed tissue repair. In this review, we summarize recent mechanistic advances in MQC-mediated regulation of lung development across fetal, preterm, and term infant models. Therapeutic strategies targeting MQC have shown promise in preclinical studies, with stem cell therapy and precision-targeted antioxidant delivery emerging as potential approaches to restore mitochondrial homeostasis and promote alveologenesis. We advocate for timely, mitochondria-centered interventions during fetal and neonatal periods to improve pulmonary outcomes and sustain lifelong respiratory health.</p>

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Mitochondrial quality control mechanisms as molecular targets for impaired lung development: from fetuses to neonates

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年12月28日

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  • Ziwei Zhu,
  • Liang Zhang,
  • Jianhua Fu

摘要

Lung development is a highly programmed and energy-dependent dynamic process, with the fetal and neonatal periods representing critical developmental windows. Emerging evidence indicates that mitochondrial quality control (MQC) mechanisms—including mitophagy, mitochondrial dynamics (fusion/fission), and mitochondrial biogenesis—play a central regulatory role in pulmonary development and injury responses during these periods. While, under stressors in the maternal-fetal environment or hyperoxia therapy, transiently upregulate MQC may serve as protective compensatory response, MQC dysregulation can lead to the accumulation of dysfunctional mitochondria, exacerbated oxidative stress, aberrant cellular metabolism, and amplified inflammatory responses. These disruptions contribute to pathological sequelae such as impaired alveolar epithelial differentiation, aberrant pulmonary vascular remodeling, diminished antioxidant capacity, and failed tissue repair. In this review, we summarize recent mechanistic advances in MQC-mediated regulation of lung development across fetal, preterm, and term infant models. Therapeutic strategies targeting MQC have shown promise in preclinical studies, with stem cell therapy and precision-targeted antioxidant delivery emerging as potential approaches to restore mitochondrial homeostasis and promote alveologenesis. We advocate for timely, mitochondria-centered interventions during fetal and neonatal periods to improve pulmonary outcomes and sustain lifelong respiratory health.