Evidence map›Paper›PMID 40745297›Full record

ArticleBMC oral health2025

Lactate inhibits mouse embryonic palatal mesenchyme cells chondrogenesis through AKT-PKM2 axis.

Mingyue Meng, Xige Zhao, Xiaoyu Zheng, Xiaotong Wang, Xia Peng, Zhiwei Wang, Shiteng Wang, Cui Guo, Juan Du

Abstract read
In one paragraph

Article in BMC oral health, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

9 authors.

Mingyue MengLaboratory of Orofacial Development, Laboratory of Molecular Signaling and Stem Cells Therapy, Molecular Laboratory for Gene Therapy and Tooth Regeneration, Beijing Key Laboratory of Tooth Regeneration and Function Reconstruction, Capital Medical University School of Stomatology, Fan Jiacun Road No. 9, Beijing, 100071, China.
Xige ZhaoLaboratory of Orofacial Development, Laboratory of Molecular Signaling and Stem Cells Therapy, Molecular Laboratory for Gene Therapy and Tooth Regeneration, Beijing Key Laboratory of Tooth Regeneration and Function Reconstruction, Capital Medical University School of Stomatology, Fan Jiacun Road No. 9, Beijing, 100071, China.
Xiaoyu ZhengLaboratory of Orofacial Development, Laboratory of Molecular Signaling and Stem Cells Therapy, Molecular Laboratory for Gene Therapy and Tooth Regeneration, Beijing Key Laboratory of Tooth Regeneration and Function Reconstruction, Capital Medical University School of Stomatology, Fan Jiacun Road No. 9, Beijing, 100071, China.
Xiaotong WangLaboratory of Orofacial Development, Laboratory of Molecular Signaling and Stem Cells Therapy, Molecular Laboratory for Gene Therapy and Tooth Regeneration, Beijing Key Laboratory of Tooth Regeneration and Function Reconstruction, Capital Medical University School of Stomatology, Fan Jiacun Road No. 9, Beijing, 100071, China.
Xia PengLaboratory of Orofacial Development, Laboratory of Molecular Signaling and Stem Cells Therapy, Molecular Laboratory for Gene Therapy and Tooth Regeneration, Beijing Key Laboratory of Tooth Regeneration and Function Reconstruction, Capital Medical University School of Stomatology, Fan Jiacun Road No. 9, Beijing, 100071, China.
Zhiwei WangLaboratory of Orofacial Development, Laboratory of Molecular Signaling and Stem Cells Therapy, Molecular Laboratory for Gene Therapy and Tooth Regeneration, Beijing Key Laboratory of Tooth Regeneration and Function Reconstruction, Capital Medical University School of Stomatology, Fan Jiacun Road No. 9, Beijing, 100071, China.
Shiteng WangLaboratory of Orofacial Development, Laboratory of Molecular Signaling and Stem Cells Therapy, Molecular Laboratory for Gene Therapy and Tooth Regeneration, Beijing Key Laboratory of Tooth Regeneration and Function Reconstruction, Capital Medical University School of Stomatology, Fan Jiacun Road No. 9, Beijing, 100071, China.
Cui GuoDepartment of Geriatric Dentistry, Capital Medical University School of Stomatology, Fanjiacun Road No. 9, Beijing, 100070, China.
Juan DuLaboratory of Orofacial Development, Laboratory of Molecular Signaling and Stem Cells Therapy, Molecular Laboratory for Gene Therapy and Tooth Regeneration, Beijing Key Laboratory of Tooth Regeneration and Function Reconstruction, Capital Medical University School of Stomatology, Fan Jiacun Road No. 9, Beijing, 100071, China. juandug@ccmu.edu.cn.

Funding

Beijing Natural Science Foundation 7252059the National Natural Science Foundation of China 82170912
6 · The paper itself

Abstract

backgroundThe development of the palate is a complex and continuous process, occurring in a series of stages with cartilage of being particular significance. Chondrogenesis is influenced by many factors such as metabolism, and hypoxia which are also risk factors for cleft palate. Hypoxia can increase the intracellular lactate levels due to increased glycolysis. However, the precise role of lactate in palatal cartilage development remains unclear.

methodsMouse embryonic palatal mesenchyme (MEPM) cells isolated from embryonic day 13.5 (E13.5) and E12.5 were obtained and characterized using immunofluorescence. Subsequently, following a 21-day induction culture in a chondrogenic medium, the MEPM cells were subjected to alcian blue staining and to quantitative real-time PCR to examine the ability of the cells to form a cartilage matrix under the influence of lactate, hypoxia, and a combination of both. The expression levels of glycolysis-related enzymes, hypoxia-inducible factor-1α (HIF-1α), and the phosphoinositide 3-kinase/AKT signaling pathway were examined using western blot and quantitative real-time PCR to investigate the mechanism of lactate in palatal cartilage development.

resultsThe findings indicated that extracellular lactate supplementation impeded the formation of cellular cartilage matrix in comparison to the control group. Then hypoxia was observed to induce intracellular lactate accumulation and also inhibited the capacity of MEPM cells to form cartilage matrix. This process was associated with an increased expression of glycolysis-related enzymes and enhanced AKT signaling pathway activity.

conclusionsThis study demonstrates that lactate can inhibit palatal cartilage development and affect the process of glycolysis. Lactate inhibits palatal cartilage matrix formation by activating the AKT-PKM2 axis. This study contributes to our understanding of the role of lactate in palatal cartilage development. It provides a new direction for the etiology of cleft palate and a theoretical basis for its prevention and early intervention.

Indexed as

Carrier ProteinsChondrogenesisLactic AcidMembrane ProteinsMesenchymal Stem CellsMesodermPalateProto-Oncogene Proteins c-aktThyroid HormonesAnimalsBlotting, WesternCells, CulturedCleft PalateGlycolysisHypoxia-Inducible Factor 1, alpha SubunitMiceCarrier ProteinsHif1a protein, mouseHypoxia-Inducible Factor 1, alpha SubunitLactic AcidMembrane ProteinsPkm protein, mouseProto-Oncogene Proteins c-aktPyruvate KinaseThyroid HormonesChondrogenesisCleft palateGlycolysisHypoxiaLactateMEPM cells

Identifiers

PMID40745297
PMCPMC12315313

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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.