2. Academic Validation
  3. Melatonin Increased Autophagy Level to Facilitate Osteogenesis of Inflamed PDLSCs Through TMEM110 Signaling Pathways

Melatonin Increased Autophagy Level to Facilitate Osteogenesis of Inflamed PDLSCs Through TMEM110 Signaling Pathways

  • J Pineal Res. 2025 Mar;77(2):e70039. doi: 10.1111/jpi.70039.
Xinyue Xu 1 2,  Zhaojia Zhang 3,  Wen Tian 3,  Meng Cao 2,  Zhen Wang 2,  Fei Li 2,  Tian Gao 2,  Mengjuan Cheng 1,  Yunlong Xia 2 4,  Jinlong Shao 5,  Chunxu Hai 2
Affiliations

Affiliations

  • 1 State Key Laboratory of Military Stomatology, National Clinical Research Center for Oral Diseases and Shaanxi Engineering Research Center for Dental Materials and Advanced Manufacture, Department of Preventive Dentistry, School of Stomatology, Fourth Military Medical University, Xi'an, P. R. China.
  • 2 Department of Toxicology, The Ministry of Education Key Lab of Hazard Assessment and Control in Special Operational Environment, Shanxi Key Lab of Free Radical Biology and Medicine, School of Public Health, The Fourth Military Medical University, Xi'an, China.
  • 3 College of Basic Medicine, Fourth Military Medical University, Xi'an, P. R. China.
  • 4 Department of Cardiology, Xijing Hospital, Fourth Military Medical University, Xi'an, P. R. China.
  • 5 Department of Periodontology, School and Hospital of Stomatology, Cheeloo College of Medicine, Shandong University & Shandong Key Laboratory of Oral Tissue Regeneration & Shandong Engineering Laboratory for Dental Materials and Oral Tissue Regeneration, Jinan, Shandong, China.
PMID: 40065592 DOI: 10.1111/jpi.70039
Abstract

Periodontal ligament stem cells (PDLSCs) bring new hope to patients with poor periodontium recovery and impaired regeneration. However, the complex inflammatory microenvironment continually inhibits stem cell function and hinders stem cell therapy effectiveness. Melatonin is a naturally occurring neurohormone that participates in the regulation of a large spectrum of biological functions. We investigated the effect of melatonin on periodontium regeneration both in vitro and in vivo. The results showed that melatonin promoted periodontitis recovery and enhanced the osteogenesis of inflamed PDLSCs (Inf-PDLSCs) depending on concentrations. Further mechanistic exploration indicated that Autophagy activation played a significant role in enhancing the osteogenic differentiation of Inf-PDLSCs after melatonin treatment. Additionally, melatonin-induced upregulation of TEME110 participated in the initiation of Autophagy activation and enhancement of osteogenesis in Inf-PDLSCs. Collectively, the results of our study provide evidence that melatonin-mediated osteogenesis of Inf-PDLSCs is important for periodontal tissue regeneration. Moreover, melatonin as a therapeutic drug for periodontitis treatment deserves further investigation.

Keywords

TMEM110; autophagy; inflammation; melatonin; osteogenesis; periodontitis.

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