Evidence map›Paper›PMID 40999515›Full record

ArticleStem cell research & therapy2025

SUV39H1 facilitate the osteogenic differentiation of dental pulp stem cells by modulating lipid metabolism and mitochondrial dynamics through FASN via non-histone methylation and ubiquitination mechanism.

Ning Wang, Wanqing Wang, Xiao Han, Yangyang Cao, Haoqing Yang, Chen Zhang, Huina Liu, Mengyuan Zhu, Dengsheng Xia, Zhipeng Fan

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Stem cell research & therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

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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

1 citing paper in PubMed.

  1. 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.

Ning Wang *Laboratory of Molecular Signaling and Stem Cells Therapy, Beijing Key Laboratory of Tooth Regeneration and Function Reconstruction, Capital Medical University School of Stomatology, Beijing, 100050, China.
Wanqing Wang *Laboratory of Molecular Signaling and Stem Cells Therapy, Beijing Key Laboratory of Tooth Regeneration and Function Reconstruction, Capital Medical University School of Stomatology, Beijing, 100050, China.
Xiao HanLaboratory of Molecular Signaling and Stem Cells Therapy, Beijing Key Laboratory of Tooth Regeneration and Function Reconstruction, Capital Medical University School of Stomatology, Beijing, 100050, China.
Yangyang CaoLaboratory of Molecular Signaling and Stem Cells Therapy, Beijing Key Laboratory of Tooth Regeneration and Function Reconstruction, Capital Medical University School of Stomatology, Beijing, 100050, China.
Haoqing YangLaboratory of Molecular Signaling and Stem Cells Therapy, Beijing Key Laboratory of Tooth Regeneration and Function Reconstruction, Capital Medical University School of Stomatology, Beijing, 100050, China.
Chen ZhangLaboratory of Molecular Signaling and Stem Cells Therapy, Beijing Key Laboratory of Tooth Regeneration and Function Reconstruction, Capital Medical University School of Stomatology, Beijing, 100050, China.
Huina LiuLaboratory of Molecular Signaling and Stem Cells Therapy, Beijing Key Laboratory of Tooth Regeneration and Function Reconstruction, Capital Medical University School of Stomatology, Beijing, 100050, China.
Mengyuan ZhuLaboratory of Molecular Signaling and Stem Cells Therapy, Beijing Key Laboratory of Tooth Regeneration and Function Reconstruction, Capital Medical University School of Stomatology, Beijing, 100050, China.
Dengsheng XiaDepartment of General Dentistry and Integrated Emergency Dental Care, Beijing Stomatological Hospital, Capital Medical University School of Stomatology, Beijing, China. xdsh1202@aliyun.com.
Zhipeng FanLaboratory of Molecular Signaling and Stem Cells Therapy, Beijing Key Laboratory of Tooth Regeneration and Function Reconstruction, Capital Medical University School of Stomatology, Beijing, 100050, China. zpfan@ccmu.edu.cn.ORCID http://orcid.org/0000-0003-1662-9420

Funding

National Natural Science Foundation of China 82130028National Natural Science Foundation of China 82270951
6 · The paper itself

Abstract

backgroundTissue engineering technology has limited application in bone tissue regeneration because the mechanism remains unclear. SUV39H1 is a well-characterized histone methyltransferase, but its specific role in bone regeneration of dental pulp stem cells(DPSCs) remains unclear. Mitochondrial energy metabolism plays a regulatory role in osteogenesis, with lipid metabolites serving as critical substrates to fuel this process. FASN has been established as a key regulator of fatty acid metabolism. Therefore, we speculate that SUV39H1 influences the osteogenic differentiation of DPSCs through the mediation of FASN. However, it is still unclear how to regulate the expression of the SUV39H1.

methodsAlkaline phosphatase activity and alizarin red staining were used to detect the osteogenic differentiation of DPSCs. Real-time reverse transcription polymerase chain reaction (RT-PCR) and Western blot were performed to detect gene expression levels. Cranioparietal bone replantation in rats and subcutaneous replantation in nude mice were used to confirm bone tissue regeneration. The Seahorse Cell Mitochondria Stress Test was used to detect the oxygen consumption rate. Co-Immunoprecipitation and GST pull-down confirmed the proteins complex. Lipid metabolism sequencing was used to detect the lipid metabolites. Software-based prediction tools analyze gene conservation and interaction networks. Dual-luciferase Reporter Gene Assay was used to detect SUV39H1 regulation by miRNA.

resultsSUV39H1 promoted osteogenic differentiation and bone regeneration in DPSCs. Our results further demonstrated that SUV39H1 enhanced the osteogenic differentiation of DPSCs by promoting lipid metabolism and subsequent mitochondrial energy metabolism. Upon exploring the mechanism by which SUV39H1 regulates lipid metabolism and mitochondrial function. SUV39H1 was found to bind to non-histone and methylated FASN. Simultaneously, FASN was degraded by ubiquitination after SUV39H1 combined with FASN. Thus, SUV39H1 was speculated to methylate FASN, and subsequently recruit a ubiquitination enzyme targeting FASN for degradation. This process modulated lipid and mitochondrial energy metabolism to facilitate the bone regeneration of DPSCs. Regarding the mechanism of regulating SUV39H1 expression, miR-4788 bound to the 3 'UTR of SUV39H1 was found to silence its expression.

conclusionOverall, SUV39H1 facilitated the osteogenic differentiation of DPSCs by modulating lipid metabolism and affected mitochondrial energy metabolism through FASN via non-histone methylation and ubiquitination mechanisms. The expression of SUV39H1was regulated by miR-4788.

Indexed as

Dental PulpFatty Acid Synthase, Type ILipid MetabolismMethyltransferasesMitochondrial DynamicsOsteogenesisRepressor ProteinsStem CellsAnimalsCell DifferentiationHumansMaleMethylationMiceMice, NudeRatsFatty Acid Synthase, Type IMethyltransferasesRepressor ProteinsSUV39H1 protein, humanDental pulp stem cells (DPSCs)FASNmiR-4788Osteogenic differentiationSUV39H1

Identifiers

PMID40999515
PMCPMC12465550

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.