Authors
Jingzhou Li, Qianyi Shi, Xinyue Sheng, Haozhen Ma, Qianyi Deng, Yifan He, Fuping Zhang, Fang Huang
Published in
Biomolecules. Volume 16. Issue 5. Apr 30, 2026. Epub Apr 30, 2026.
Abstract
The differentiation of dental papilla cells (DPCs) into functional odontoblasts is critical for dentinogenesis, yet the role of mitochondrial dynamics remains unclear. Here, we investigated the functional role of mitochondrial fission and mitochondria-associated endoplasmic reticulum membranes (MAMs) in the odontogenic differentiation of DPCs. Using in vitro differentiation models combined with confocal microscopy, transmission electron microscopy, and gain- and loss-of-function approaches, we found that odontogenic induction triggered early mitochondrial fragmentation and increased MAM formation. Dynamin-related protein 1 (DRP1) mediated mitochondrial fission, which in turn regulated MAM architecture and promoted differentiation. Malic enzyme 2 (ME2) acted as an upstream regulator, facilitating DRP1 recruitment and organizing MAM integrity. Notably, disruption of the ME2-DRP1-MAM axis impaired dentin formation both in vitro and in vivo, either by ME2 knockdown or pharmacological inhibition of DRP1 (Mdivi-1). These findings establish the ME2-DRP1-MAM axis as a critical metabolic-organellar switch driving odontoblast differentiation, providing new mechanistic insights into dentinogenesis and identifying potential therapeutic targets for dentin-pulp complex regeneration.
PMID:
42194014
Bibliographic data and abstract were imported from PubMed on 13 Sep 2026.
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