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Mitochondrial programmed cell death in bronchopulmonary dysplasia: mechanisms and therapeutic targets
Jianfeng Jiang1, Mingyan Wang1, Huici Yao1
1Department of Pediatrics, The Affiliated Hospital of Jiangsu University, Zhenjiang, China.
Insights
Mitochondrial dysfunction and programmed cell death pathways disrupt lung development in premature infants with bronchopulmonary dysplasia (BPD). Therapies targeting these pathways offer new hope for treating this chronic lung disease.
Area of Science:
- Pulmonary Medicine
- Cell Biology
- Neonatology
Background:
- Bronchopulmonary dysplasia (BPD) is a major cause of chronic lung disease in preterm infants.
- Normal lung development relies on mitochondrial function and cellular homeostasis.
- Mitochondrial dysfunction is a key feature in BPD pathogenesis.
Purpose of the Study:
- To review the role of mitochondrial dysfunction in BPD.
- To examine the interconnected programmed cell death pathways in BPD.
- To discuss emerging therapeutic strategies for BPD.
Main Methods:
- Literature review of mitochondrial dysfunction in BPD.
- Analysis of programmed cell death pathways (mitophagy, apoptosis, necroptosis, pyroptosis, ferroptosis) in pulmonary cells.
- Examination of therapeutic approaches including mitochondrial restoration and regenerative medicine.
Main Results:
- BPD involves disrupted mitochondrial homeostasis (fission/fusion imbalance, impaired biogenesis, altered mitophagy, oxidative stress, energy deficit).
- Multiple programmed cell death pathways are activated and crosstalk in pulmonary cells, hindering lung development.
- These pathways collectively impair cell survival, proliferation, and differentiation, arresting alveolarization and vascular development.
Conclusions:
- Mitochondrial dysfunction and complex cell death signaling are central to BPD pathogenesis.
- Targeting these pathways and restoring mitochondrial function are promising therapeutic avenues.
- Regenerative strategies, such as exosome-based delivery, show potential for BPD treatment.
Abstract:
Bronchopulmonary dysplasia (BPD) is a prevalent chronic lung disease in preterm infants, primarily characterized by arrested alveolarization and dysregulated pulmonary microvascular development. Mitochondria are crucial for normal lung development, supporting cellular energy and homeostasis. In BPD, mitochondrial homeostasis is severely disrupted, characterized by excessive fission, suppressed fusion, deficient biogenesis, imbalanced mitophagy, a collapsed antioxidant system, and a consequent energy crisis. Following mitochondrial damage, a spectrum of mitochondria-associated programmed cell death pathways is activated in pulmonary cells, including mitophagy-dependent death, apoptosis, necroptosis, pyroptosis, and ferroptosis. Within alveolar epithelial cells, vascular endothelial cells, and other pulmonary cells, these death pathways operate both independently and through extensive crosstalk, forming a complex regulatory network. This network synergistically disrupts pulmonary cell survival, proliferation, and differentiation, ultimately arresting lung development. Therapeutic strategies aim to restore mitochondrial homeostasis, inhibit specific death pathways, and utilize regenerative approaches like exosome-based delivery. This review examines the role of mitochondrial dysfunction and interconnected cell death pathways in BPD pathogenesis and discusses emerging treatments.
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