Evidence map›Paper›PMID 42717476›Full record

ArticleJournal of cellular and molecular medicine2026

METTL3 Promotes Lipid Deposition and Pulmonary Fibrosis by Destabilizing PLIN2 in a m6A-Dependent Manner.

Qiping Liu, Rui Xu, Xianzhi Du

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In one paragraph

Article in Journal of cellular and molecular medicine, 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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0citing papers in PubMed
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1 · What the graph read from it

What it found

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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.

2 · The registry

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3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors.

Qiping LiuDepartment of Respiratory and Critical Care Medicine, Second Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Rui XuDepartment of Respiratory and Critical Care Medicine, Second Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Xianzhi DuDepartment of Respiratory and Critical Care Medicine, Second Affiliated Hospital of Chongqing Medical University, Chongqing, China.

Funding

Future Medicine Youth Innovation Team Project of Chongqing Medical University W0118General Program of Chongqing Natural Science Foundation cstc2021jcyj-msxmX0216Joint General Program of Chongqing Science and Health Research 2022MSXM144
6 · The paper itself

Abstract

Idiopathic pulmonary fibrosis (IPF) is a lethal lung disorder that is associated with aberrant lipid metabolism. N6-methyladenosine (m6A) methylation is involved in IPF progression. However, whether METTL3, a m6A methyltransferase, modulates lipid metabolism in IPF remains unknown. In this study, we aimed to investigate the effects of METTL3 on fibrosis and lipid accumulation and identify the molecular mechanism. PF mouse model was generated by bleomycin. WI-38 cells were stimulated with TGF-β1 to mimic the IPF-caused damage. Lipids were observed using Nile Red staining and marker detection. Fibrosis was evaluated using Masson's Trichrome staining and marker detection. The molecular mechanism was analysed by methylated RNA immunoprecipitation and dual-luciferase reporter assay. We found that METTL3 is highly expressed in IPF mice and TGF-β1-induced WI-38 cells. Knockdown of METTL3 inhibited lipid accumulation and fibrosis In Vitro and In Vivo. Additionally, interference with METTL3 suppressed the m6A methylation of PLIN2, enhanced its stability, and increased its expression. Knockdown of PLIN2 reversed the inhibition of lipid accumulation and fibrosis caused by METTL3 silence. In conclusion, interfering with METTL3 attenuates IPF progression by suppressing lipid deposition, which is associated with the increased stability of PLIN2 suggesting a promising therapeutic target for IPF.

Indexed as

AdenosineIdiopathic Pulmonary FibrosisLipid MetabolismMethyltransferasesPerilipin-2AnimalsCell LineDisease Models, AnimalEpitranscriptomeHumansMaleMiceRNA MethylationTransforming Growth Factor beta1AdenosineMethyltransferasesMETTL3 protein, humanMettl3 protein, mouseN-methyladenosinePerilipin-2Plin2 protein, mouseTransforming Growth Factor beta1idiopathic pulmonary fibrosislipidm6A methylationMETTL3PLIN2

Identifiers

PMID42717476
PMCPMC13558835

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.