ArticleClinics (Sao Paulo, Brazil)2023
METTL3 promotes hyperoxia-induced pyroptosis in neonatal bronchopulmonary dysplasia by inhibiting ATG8-mediated autophagy.
Article in Clinics (Sao Paulo, Brazil), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 9 citations in OpenAlex.
- Epigenetic programming in bronchopulmonary dysplasia: a framework linking early-life exposures to persistent lung disease-a narrative review.Pediatric research · 2026Review
- Mitochondrial programmed cell death in bronchopulmonary dysplasia: mechanisms and therapeutic targets.Frontiers in physiology · 2026Review
- METTL3 aggravates lung injury in neonatal mice withInfection and immunity · 2025Article
- Establishment and Evaluation of Cell Models for Bronchopulmonary Dysplasia: Challenges and Prospects.The clinical respiratory journal · 2025Review
- Decoding bronchopulmonary dysplasia in premature infants through an epigenetic lens.Frontiers in medicine · 2025Review
- Lutein Alleviate Acute Lung Injury Induced by Limb Ischemia-Reperfusion Through PPAR-γ/PI3K/AKT/NLRP3 Signaling.Mediators of inflammation · 2025Article
- Development and validation of the prediction model based on autophagy-associated genes in bronchopulmonary dysplasia.Annals of medicine · 2024Article
- Methyltransferase-Like 3-Mediated N6-Methyladenosine RNA Methylation Regulates Hypoxia-Induced Pulmonary Arterial Smooth Muscle Cell Pyroptosis by Targeting PTEN.Journal of the American Heart Association · 2024Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesN6-Methyladenosine (m6A) modification plays a vital role in lung disorders. However, the potential of m6A in neonatal Bronchopulmonary Dysplasia (BPD) has not been reported. This study aimed to investigate the roles of METTL3 in BPD.
methodsBPD models were established by hyperoxia in vivo and in vitro. Histological analysis was determined using HE staining. Gene expression was determined using Western blotting, qRT-PCR, and immunofluorescence. The release of IL-1β and IL-18 was detected using ELISA. The m6A sites of ATG8 were predicted by SCRAPM and verified by MeRIP assay. The location of GSDMD and ATG8 was determined by FISH assay. The interaction between ATG8 and GSDMD was detected using Coimmunoprecipitation (Co-IP). Cell pyroptosis was determined using flow cytometry and TUNEL assays.
resultsMETTL3 was overexpressed in BPD, which was accompanied by an increase in m6A levels. Interestingly, METTL3 suppressed hyperoxia-mediated damage and pyroptosis in BEAS-2B cells and promoted cell autophagy. METTL3-mediated m6A modification of ATG8 suppressed its expression and disrupted the interaction between ATG8 and GSDMD. However, autophagy inhibition induced pyroptosis in BEAS-2B cells. In vivo assays showed that METTL3-mediated autophagy inhibition induced a decrease in the radial alveolar count and an increase in the mean linear intercept and promoted cell pyroptosis.
conclusionIn conclusion, METTL3-mediated cell pyroptosis promotes BPD by regulating the m6A modification of ATG8. This may provide new insight into the development of BPD.
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