ReviewFrontiers in physiology2026
Mitochondrial programmed cell death in bronchopulmonary dysplasia: mechanisms and therapeutic targets.
Review in Frontiers in physiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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5 authors.
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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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