ArticleJCI insight2023
Thyroid hormone modulates hyperoxic neonatal lung injury and mitochondrial function.
Article in JCI insight, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 10 citations in OpenAlex.
- OTULIN protects hyperoxia-induced neonatal lung injury and modulates mitochondrial protein OPA1 in association with the E3 ubiquitin ligase RNF31.Cellular & molecular biology letters · 2026Article
- Relationship between thyroid hormones and bronchopulmonary dysplasia in extremely and very preterm infants.Frontiers in physiology · 2026Article
- Effects of 3,3',5-triiodothyronine supplementation during ex vivo lung perfusion on ischemia/reperfusion injury in rat lungs.Frontiers in medicine · 2026Article
- Mitochondrial quality control mechanisms as molecular targets for impaired lung development: from fetuses to neonates.Respiratory research · 2025Review
- Protective Action of 3,5-Diiodo-L-Thyronine on Cigarette Smoke-Induced Mitochondrial Dysfunction in Human Alveolar Epithelial Cells.Biomedicines · 2025Article
- Assessing the impact of triiodothyronine treatment on the lung microbiome of mice with pulmonary fibrosis.BMC pulmonary medicine · 2024Article
- Case Report: Diagnosis of Hyperthyroidism in a Preterm Infant With Concurrent Respiratory Distress Syndrome.AACE endocrinology and diabetesArticle
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Mitochondrial dysfunction at birth predicts bronchopulmonary dysplasia (BPD) in extremely low-birth weight (ELBW) infants. Recently, nebulized thyroid hormone (TH), given as triiodothyronine (T3), was noted to decrease pulmonary fibrosis in adult animals through improved mitochondrial function. In this study, we tested the hypothesis that TH may have similar effects on hyperoxia-induced neonatal lung injury and mitochondrial dysfunction by testing whether i.n. T3 decreases neonatal hyperoxic lung injury in newborn mice; whether T3 improves mitochondrial function in lung homogenates, neonatal murine lung fibroblasts (NMLFs), and umbilical cord-derived mesenchymal stem cells (UC-MSCs) obtained from ELBW infants; and whether neonatal hypothyroxinemia is associated with BPD in ELBW infants. We found that inhaled T3 (given i.n.) attenuated hyperoxia-induced lung injury and mitochondrial dysfunction in newborn mice. T3 also reduced bioenergetic deficits in UC-MSCs obtained from both infants with no or mild BPD and those with moderate to severe BPD. T3 also increased the content of peroxisome proliferator-activated receptor γ coactivator 1α in lung homogenates of mice exposed to hyperoxia as well as mitochondrial potential in both NMLFs and UC-MSCs. ELBW infants who died or developed moderate to severe BPD had lower total T4 (TT4) compared with survivors with no or mild BPD. In conclusion, TH signaling and function may play a critical role in neonatal lung injury, and inhaled T3 supplementation may be useful as a therapeutic strategy for BPD.
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