Evidence map›Paper›PMID 41748932›Full record

ArticleCellular and molecular life sciences : CMLS2026

IMP2 enhances M2 macrophage polarization via LKB1-AMPK-mediated mitochondrial dynamics and fatty acid β-oxidation to ameliorate diabetic osteoporosis.

Lingshuang Li, Yajun Cui, Yu Ji, Ke Ma, Xuejie Lin, Ting Liu, Junyang Sun, Hongrui Liu, Jie Guo, Minqi Li

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cellular and molecular life sciences : CMLS, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. Review
  2. Review
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

10 authors.

Lingshuang LiDepartment of Bone Metabolism, School and Hospital of Stomatology, Cheeloo College of Medicine, Shandong Key Laboratory of Oral Tissue Regeneration & Shandong Engineering Research Center of Dental Materials and Oral Tissue Regeneration & Shandong Provincial Clinical Research Center for Oral Diseases, Shandong University, Jinan, China.
Yajun CuiDepartment of Bone Metabolism, School and Hospital of Stomatology, Cheeloo College of Medicine, Shandong Key Laboratory of Oral Tissue Regeneration & Shandong Engineering Research Center of Dental Materials and Oral Tissue Regeneration & Shandong Provincial Clinical Research Center for Oral Diseases, Shandong University, Jinan, China.
Yu JiDepartment of Bone Metabolism, School and Hospital of Stomatology, Cheeloo College of Medicine, Shandong Key Laboratory of Oral Tissue Regeneration & Shandong Engineering Research Center of Dental Materials and Oral Tissue Regeneration & Shandong Provincial Clinical Research Center for Oral Diseases, Shandong University, Jinan, China.
Ke MaDepartment of Bone Metabolism, School and Hospital of Stomatology, Cheeloo College of Medicine, Shandong Key Laboratory of Oral Tissue Regeneration & Shandong Engineering Research Center of Dental Materials and Oral Tissue Regeneration & Shandong Provincial Clinical Research Center for Oral Diseases, Shandong University, Jinan, China.
Xuejie LinDepartment of Bone Metabolism, School and Hospital of Stomatology, Cheeloo College of Medicine, Shandong Key Laboratory of Oral Tissue Regeneration & Shandong Engineering Research Center of Dental Materials and Oral Tissue Regeneration & Shandong Provincial Clinical Research Center for Oral Diseases, Shandong University, Jinan, China.
Ting LiuDepartment of Bone Metabolism, School and Hospital of Stomatology, Cheeloo College of Medicine, Shandong Key Laboratory of Oral Tissue Regeneration & Shandong Engineering Research Center of Dental Materials and Oral Tissue Regeneration & Shandong Provincial Clinical Research Center for Oral Diseases, Shandong University, Jinan, China.
Junyang SunDepartment of Bone Metabolism, School and Hospital of Stomatology, Cheeloo College of Medicine, Shandong Key Laboratory of Oral Tissue Regeneration & Shandong Engineering Research Center of Dental Materials and Oral Tissue Regeneration & Shandong Provincial Clinical Research Center for Oral Diseases, Shandong University, Jinan, China.
Hongrui LiuDepartment of Bone Metabolism, School and Hospital of Stomatology, Cheeloo College of Medicine, Shandong Key Laboratory of Oral Tissue Regeneration & Shandong Engineering Research Center of Dental Materials and Oral Tissue Regeneration & Shandong Provincial Clinical Research Center for Oral Diseases, Shandong University, Jinan, China. yf1blhr@126.com.
Jie GuoDepartment of Bone Metabolism, School and Hospital of Stomatology, Cheeloo College of Medicine, Shandong Key Laboratory of Oral Tissue Regeneration & Shandong Engineering Research Center of Dental Materials and Oral Tissue Regeneration & Shandong Provincial Clinical Research Center for Oral Diseases, Shandong University, Jinan, China. kqgj@sdu.edu.cn.
Minqi LiDepartment of Bone Metabolism, School and Hospital of Stomatology, Cheeloo College of Medicine, Shandong Key Laboratory of Oral Tissue Regeneration & Shandong Engineering Research Center of Dental Materials and Oral Tissue Regeneration & Shandong Provincial Clinical Research Center for Oral Diseases, Shandong University, Jinan, China. liminqi@sdu.edu.cn.ORCID http://orcid.org/0000-0001-9980-1382

Funding

Construction Engineering Special Fund of "Taishan Young Scholars" of Shandong Province tsqn202103177National Natural Science Foundation of China 82370999Natural Science Foundation of Shandong Province ZR202210210042Taishan Scholar Foundation of Shandong Province No. tstp20221160
6 · The paper itself

Abstract

A reduction in M2 macrophage polarization is a key pathogenic contributor to diabetic osteoporosis (DOP). In this study, we revealed that IMP2 affects mitochondrial dynamics and fatty acid β-oxidation (FAO) via the LKB1-AMPK pathway, influencing the M2 polarization pattern and thereby improving DOP. Leveraging Cre-loxp technology, we generated macrophage-specific IMP2 knockout mice. Under diabetic settings, IMP2 knockout further disrupted M2 macrophage polarization and intensified bone deterioration. Mechanistically, IMP2 enhances LKB1 mRNA stability through the N6-methyladenosine (m6A) pathway, activating the LKB1-AMPK signaling cascade. This pathway promotes mitochondrial fusion and boosts FAO, fueling M2 macrophage polarization. Enhanced M2 polarization, in turn bolsters the osteogenic differentiation potential of bone marrow mesenchymal stem cells (BMSCs). However, in the diabetic milieu, IMP2’s regulatory role in M2 macrophages is compromised, diminishing the osteogenic support provided by M2 macrophages to BMSCs and exacerbating bone loss.

Indexed as

AMP-Activated Protein KinasesDiabetes Mellitus, ExperimentalFatty AcidsMacrophagesMitochondrial DynamicsOsteoporosisProtein Serine-Threonine KinasesRNA-Binding ProteinsAMP-Activated Protein Kinase KinasesAnimalsCell DifferentiationMesenchymal Stem CellsMiceMice, Inbred C57BLMice, KnockoutOsteogenesisAMP-Activated Protein Kinase KinasesAMP-Activated Protein KinasesFatty AcidsIGF2BP2 protein, mouseProtein Serine-Threonine KinasesRNA-Binding ProteinsStk11 protein, mouseAMPKDiabetic osteoporosisFatty acid β-oxidationIMP2LKB1M6AMitochondrial dynamics

Identifiers

PMID41748932
PMCPMC12961074

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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Registered trials

None linked

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 Socratic graph.