ArticleTranslational pediatrics2021
Long non-coding RNA MALAT1 plays a protective role in bronchopulmonary dysplasia via the inhibition of apoptosis and interaction with the Keap1/Nrf2 signal pathway.
Article in Translational pediatrics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 16 citations in OpenAlex.
- The Prospective Regulatory Functions of lncRNAs and Their ceRNA Networks in the Development of Motor Neurons and Associated Diseases.Biomolecules · 2026Review
- Oxidative Stress, Environmental Pollutants, Aging, and Epigenetic Regulation: Mechanistic Insights and Biomarker Advances.Antioxidants (Basel, Switzerland) · 2026Review
- When stress exceeds developmental capacity: rethinking cell death in bronchopulmonary dysplasia.Frontiers in pediatrics · 2026Article
- Mitochondria as the central regulator of cell death in bronchopulmonary dysplasia.Frontiers in physiology · 2025Review
- Epigenetic modifications in the development of bronchopulmonary dysplasia: a review.Pediatric research · 2024Review
- Recruitment of PVT1 Enhances YTHDC1-Mediated m6A Modification of IL-33 in Hyperoxia-Induced Lung Injury During Bronchopulmonary Dysplasia.Inflammation · 2024Article
- Regulating NLRP3 Inflammasome-Induced Pyroptosis via Nrf2: TBHQ Limits Hyperoxia-Induced Lung Injury in a Mouse Model of Bronchopulmonary Dysplasia.Inflammation · 2023Article
- Molecular mechanisms of cell death in bronchopulmonary dysplasia.Apoptosis : an international journal on programmed cell death · 2023Review
- Oxygen toxicity: cellular mechanisms in normobaric hyperoxia.Cell biology and toxicology · 2023Review
- Mechanistic studies of MALAT1 in respiratory diseases.Frontiers in molecular biosciences · 2022Review
- Focus on long non-coding RNA MALAT1: Insights into acute and chronic lung diseases.Frontiers in genetics · 2022Review
- Protective effect of adrenomedullin on hyperoxia-induced lung injury.Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2021Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundBronchopulmonary dysplasia (BPD) is a common respiratory disease in premature infants and is characterized by alveolar and pulmonary vascular dysplasia. Long-term oxygen exposure can cause BPD in preterm infants. Numerous studies have shown that long non-coding ribonucleic acid (lncRNA) is involved in the process of biological metabolism; however, its role in the development of BPD is unclear. Apoptosis-induced factor (AIF) is a key component involved in apoptosis. The Kelch-like ECH-associated protein 1/nuclear factor erythroid-2-related factor 2 (Keap1/Nrf2) signaling pathway is a body-derived antioxidant signaling pathway.
methodsIn this study, the relative expression of metastasis-associated lung adenocarcinoma transcript 1 (MALAT1), AIF, Keap1, and Nrf2 was detected by real-time polymerase chain reaction (PCR). Also, the apoptosis of A549 cells was detected by flow cytometry.
resultsThe results showed that, compared to the control group, the expression of MALAT1 increased significantly, and AIF decreased substantially in BPD premature infants. In the A549 hyperoxic lung injury model, compared with the air group, the expression of MALAT1 in the hyperoxia group decreased markedly, while the expression of Keap1 and Nrf2 increased considerably. Furthermore, compared with the control plasmid transfection air group (NC group), the expression of Keap1 and Nrf2 increased significantly in the small interfering RNA (siRNA) group.
conclusionsThese results indicate that MALAT1 can play a protective role in BPD via the reduction of apoptosis and anti-oxidation, offering clinicians a new way to prevent and treat BPD.
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