Evidence map›Paper›PMID 40672621›Full record

ArticleAmerican journal of translational research2025

Undemineralized dentin matrix particles accelerate blood vessel formation in a critical-sized skull defect through activating the TGF-β/PI3K signaling pathway.

Wei Zu, Xiangwen Zhou, Qingsong Jiang

Abstract read
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Article in American journal of translational research, 2025. 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

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

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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

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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.

Wei ZuBeijing Stomatological Hospital, Capital Medical University, Capital Medical University School of Stomatology Beijing 100070, China.
Xiangwen ZhouBeijing Stomatological Hospital, Capital Medical University, Capital Medical University School of Stomatology Beijing 100070, China.
Qingsong JiangBeijing Stomatological Hospital, Capital Medical University, Capital Medical University School of Stomatology Beijing 100070, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveTo evaluate the effects of undemineralized dentin matrix (UDDM) particles on bone tissue regeneration and vascularization in a critical-sized skull defect (CSD) mouse model, and to elucidate the molecular mechanisms underlying UDDM extract-mediated promotion of endothelial cell proliferation, migration, and tube formation.

methodsUDDM particles and extracts were sourced from human third molars. A CSD mouse model was established, and UDDM particles were implanted into the defect site. Bone regeneration and vascularization (blood vessel volume and area) were assessed using micro-computed tomography (Micro-CT). Human umbilical vein endothelial cells (HUVECs) were treated with UDDM extract and a phosphatidylinositol 3-kinase (PI3K) inhibitor (HY-15244). Cell proliferation, migration, and tube formation were assessed. Reverse transcription quantitative polymerase chain reaction (RT-qPCR) and western blot were used to analyze the expression of transforming growth factor-beta (TGF-β)/PI3K signaling pathway-related genes and proteins.

resultsUDDM particles significantly enhanced bone formation and increased vascular volume and area in the CSD model. UDDM extract promoted HUVEC proliferation, migration, and tube formation, which were reversed by HY-15244 treatment. HY-15244 also inhibited the mRNA and protein expression of TGF-β/PI3K pathway components, which were partially rescued by UDDM extract.

conclusionUDDM particles promote bone tissue regeneration and angiogenesis in a CSD mouse model. UDDM extract facilitates proliferation, migration, and tube formation of HUVECs by activating the TGF-β/PI3K signaling pathway. These findings suggest that UDDM particles and extracts hold promise for therapeutic application in bone defect repair and vascularization.

Indexed as

blood vessel formationcritical-sized skull defectHUVECTGF-β/PI3K signaling pathwayUndemineralized dentin matrix

Identifiers

PMID40672621
PMCPMC12261147

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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.