Level D· Scientific groundwork from lab and animal studiesAnimal StudyEurope PMCOpen access

Mitochondrial transplant activates Ca<sup>2+</sup>/TFAP2A to promote hDPSCs-mediated dentin-pulp regeneration

Zhan P., Zhang X., Xie Z., Chen L., Huang S., Huang Q.

Animal Study, published in Stem Cell Res Ther (2026) — summary generated from the PubMed abstract.

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Level D· Scientific groundwork from lab and animal studiesEvidence level of this study

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

  • Level A · Stronger Clinical Evidence
  • Level B · Emerging clinical evidence with positive signals
  • Level C · Early human research exploring benefits
  • Level D · Scientific groundwork from lab and animal studies
  • Emerging · Emerging topic under active research
Read the A–D evidence level guide

This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.

Study type
Animal Study
Journal
Stem Cell Res Ther (2026)
Reported sample size
—
Source database
Europe PMC
PMID
41827079
PMCID
PMC13097647
DOI
10.1186/s13287-026-04949-y

Abstract (original English)

Background The dentin-pulp complex (DPC) is composed of the odontoblastic layer and associated stromal components. It serves key functions in immunological homeostasis and tissue regeneration of dental tissues. Human dental pulp stem cells (hDPSCs) have emerged as pivotal cells for DPC regeneration. Current research frontiers primarily focus on developing novel strategies to increase the odontogenic differentiation potential and regenerative efficacy of hDPSCs. This study aims to boost the capacity of hDPSCs to regenerate DPC through mitochondrial transplantation. Methods Mitochondria were isolated from donor hDPSCs and transplanted into recipient hDPSCs (Mito-hDPSCs) in the same passage. Subsequently, cell viability and mitochondrial transplantation efficiency were evaluated via CCK-8, β-galactosidase staining, mitochondrial imaging, and flow cytometry. Furthermore, Mito-hDPSCs' metabolic capacity was assessed by mitochondrial membrane potential assays and cellular oxidative phosphorylation assays. Moreover, Alkaline Phosphatase (ALP) activity, Alizarin Red S (ARS) staining, RT-qPCR, and Western blotting (WB) were performed to assess Mito-hDPSC's odontogenic differentiation potential. Moreover, a nude mouse model was used to assess how Mito-hDPSCs induce DPC regeneration in vivo. RNA-Seq analysis was conducted to examine the expression of signaling pathways in Mito-hDPSCs. In

What this study does not prove

  • • This study does not prove SVF is an approved treatment or a replacement for standard care.
  • • This is preclinical work; animal or laboratory results cannot be applied to humans.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

How we grade evidence
Cells, CulturedMitochondriaStem CellsDental PulpDentinAnimalsHumansMiceMice, NudeCalcium

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