The Emerging Role of METTL3 in Lung Diseases
Dong Y., Liu Y., Marciano D., Nefzi A., Black SM., Wang T.
Narrative Review, published in Int J Mol Sci (2025) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Narrative Review
- Journal
- Int J Mol Sci (2025)
- Reported sample size
- —
- Source database
- Europe PMC
- PMID
- 41515964
- PMCID
- PMC12785421
- DOI
- 10.3390/ijms27010085
Abstract (original English)
N6-methyladenosine (m 6 A) represents the most abundant and tightly controlled modification within eukaryotic mRNA, critically influencing RNA metabolism and function. The m 6 A methyltransferase Like-3 (METTL3), responsible for the complex's catalytic function, has emerged as a central epitranscriptomic regulator governing mRNA stability, alternative splicing, nuclear export, and the efficiency of mRNA translation. Converging research shows that METTL3 is involved in the pathogenesis of numerous disorders via m 6 A-dependent, post-transcriptional regulation of gene programs controlling cell growth, migration, and immune pathways. Regarding pulmonary pathophysiology, METTL3-mediated m 6 A is tied to disease initiation and progression in conditions such as asthma, chronic obstructive pulmonary disease (COPD), idiopathic pulmonary fibrosis (IPF), lung infections, acute respiratory distress syndrome (ARDS). This review summarizes the contemporary evidence for METTL3's roles and regulatory network in diverse pulmonary pathologies. We further highlight emerging strategies for targeting METTL3 as a potential therapeutic approach, underscoring its promise as a novel epitranscriptomic target. Beyond inflammatory and fibrotic disorders, we also summarize emerging evidence linking METTL3 to lung cancer and briefly outline other respiratory conditions (e.g., ILD, bronchiectasis, and secon
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is a narrative review: it collects no new patient data and does not systematically appraise evidence quality.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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