Evidence map›Paper›PMID 35980318›Full record

ArticleStem cells translational medicine2022

METTL14 Regulates Osteogenesis of Bone Marrow Mesenchymal Stem Cells via Inducing Autophagy Through m6A/IGF2BPs/Beclin-1 Signal Axis.

Mingyu He, Hong Lei, Xiaoqi He, Ying Liu, Ao Wang, Zijing Ren, Xiaoyan Liu, Gege Yan, Wenbo Wang, Yang Wang and 9 more

Open access · goldAbstract read
In one paragraph

Article in Stem cells translational medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed
7.1field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

62 citing papers in PubMed, 92 citations in OpenAlex.

  1. Article
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  4. mMolecular medicine reports · 2026
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  13. METTL14 MediatesRedox report : communications in free radical research · 2025
    Article
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2 more citing papers are in PubMed but not listed here.

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

19 authors at 1 institution in 1 country.

Mingyu HeDepartment of Pharmacology, College of Pharmacy, Harbin Medical University, Harbin, People's Republic of China.
Hong LeiDepartment of Pharmacology, College of Pharmacy, Harbin Medical University, Harbin, People's Republic of China.
Xiaoqi HeDepartment of Pharmacology, College of Pharmacy, Harbin Medical University, Harbin, People's Republic of China.
Ying LiuDepartment of Pharmacology, College of Pharmacy, Harbin Medical University, Harbin, People's Republic of China.
Ao WangDepartment of Pharmacy (The University Key Laboratory of Drug Research, Heilongjiang Province), The Second Affiliated Hospital of Harbin Medical University, Harbin, People's Republic of China.
Zijing RenDepartment of Pharmacology, College of Pharmacy, Harbin Medical University, Harbin, People's Republic of China.
Xiaoyan LiuDepartment of Orthopedics, The First Affiliated Hospital of Harbin Medical University, Harbin, People's Republic of China.
Gege YanDepartment of Pharmacology, College of Pharmacy, Harbin Medical University, Harbin, People's Republic of China.
Wenbo WangDepartment of Orthopedics, The First Affiliated Hospital of Harbin Medical University, Harbin, People's Republic of China.
Yang WangDepartment of Pharmacy (The University Key Laboratory of Drug Research, Heilongjiang Province), The Second Affiliated Hospital of Harbin Medical University, Harbin, People's Republic of China.
Guanghui LiDepartment of Pharmacology, College of Pharmacy, Harbin Medical University, Harbin, People's Republic of China.
Tong WangDepartment of Pharmacology, College of Pharmacy, Harbin Medical University, Harbin, People's Republic of China.
Jiaying PuDepartment of Pharmacy (The University Key Laboratory of Drug Research, Heilongjiang Province), The Second Affiliated Hospital of Harbin Medical University, Harbin, People's Republic of China.
Zhihua ShenDepartment of Pharmacy (The University Key Laboratory of Drug Research, Heilongjiang Province), The Second Affiliated Hospital of Harbin Medical University, Harbin, People's Republic of China.
Yanquan WangDepartment of Pharmacology, College of Pharmacy, Harbin Medical University, Harbin, People's Republic of China.
Jiajie XieDepartment of Pharmacy (The University Key Laboratory of Drug Research, Heilongjiang Province), The Second Affiliated Hospital of Harbin Medical University, Harbin, People's Republic of China.
Weijie DuDepartment of Pharmacology, College of Pharmacy, Harbin Medical University, Harbin, People's Republic of China.
Ye YuanDepartment of Pharmacy (The University Key Laboratory of Drug Research, Heilongjiang Province), The Second Affiliated Hospital of Harbin Medical University, Harbin, People's Republic of China.ORCID 0000-0003-4822-8779
Lei YangDepartment of Orthopedics, The First Affiliated Hospital of Harbin Medical University, Harbin, People's Republic of China.
Harbin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The development of osteoporosis is often accompanied by autophagy disturbance, which also causes new osteoblast defects from bone marrow mesenchymal stem cells (BMSCs). However, the underlying molecular mechanisms are still not fully understood. Methyltransferase-like 14 (METTL14) is the main enzyme for N6-methyladenosine (m6A), the most prevalent internal modification in mammalian mRNAs, and it has been implicated in many bioprocesses. Herein, we demonstrate that METTL14 plays a critical role in autophagy induction and hinders osteoporosis process whose expression is decreased both in human osteoporosis bone tissue and ovariectomy (OVX) mice. In vivo, METTL14+/- knockdown mice exhibit elevated bone loss and impaired autophagy similar to the OVX mice, while overexpression of METTL14 significantly promotes bone formation and inhibits the progression of osteoporosis caused by OVX surgery. In vitro, METTL14 overexpression significantly enhances the osteogenic differentiation ability of BMSCs through regulating the expression of beclin-1 depending on m6A modification and inducing autophagy; the opposite is true with METTL14 silencing. Subsequently, m6A-binding proteins IGF2BP1/2/3 recognize m6A-methylated beclin-1 mRNA and promote its translation via mediating RNA stabilization. Furthermore, METTL14 negatively regulates osteoclast differentiation. Collectively, our study reveals the METTL14/IGF2BPs/beclin-1 signal axis in BMSCs osteogenic differentiation and highlights the critical roles of METTL14-mediated m6A modification in osteoporosis.

Indexed as

AutophagyMesenchymal Stem CellsMethyltransferasesOsteoporosisAnimalsBeclin-1Bone Marrow CellsCell DifferentiationFemaleHumansMiceOsteogenesisRNA, MessengerBeclin-1MethyltransferasesMETTL14 protein, humanMettl14 protein, mouseRNA, Messengerautophagybone marrow mesenchymal stem cellsm6A RNA methylationMETTL14osteogenic differentiation

Identifiers

PMID35980318
PMCPMC9492283
OpenAlexW4293825553

What OpenQuestion holds

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Registered trials

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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.