ArticleInternational dental journal2025
Serum Starvation Regulates Autophagy of Human Periodontal Ligament Cells Through Reactive Oxygen Species Mediated Adenosine Monophosphate-Activated Protein Kinase/Mechanistic Target of RAPAMYCIN Axis.
Article in International dental journal, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Lipid Metabolic Reprogramming in Periodontitis-Associated Alveolar Bone Remodeling: Mechanisms, Signaling Pathways, and Therapeutic Implications.Biomolecules · 2026Review
- Melatonin Rescues Enamel Defects Induced by Maternal Circadian Disruption via Targeting the BMAL1-JNK3 Axis.International dental journal · 2026Article
- Protein Kinase R-like Endoplasmic Reticulum Kinase-Mediated ER-Mitochondria Coupling Regulates Odontogenic Differentiation of Human Dental Pulp Stem Cells Under Inflammatory Stimuli.International dental journal · 2026Article
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Authors and funding
5 authors.
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Abstract
INTRODUCTION AND
aimsHuman periodontal ligament cells (hPDLCs) play a pivotal role in periodontal tissue remodelling, a process essential for orthodontic tooth movement (OTM). Autophagy, a survival mechanism under cellular stress, is induced by nutrient deprivation and impacts hPDLC function. This study aimed to explore the role of autophagy in the adaptive response of hPDLCs to nutritional stress, an environment simulating conditions during OTM.
methodsNutrient deprivation in hPDLCs was modelled through serum starvation. Autophagy levels and relevant markers were assessed using electron microscopy, protein assays, and gene expression analyses. Emphasis was placed on adenosine monophosphate-activated protein kinase (AMPK) signalling, specifically phosphorylation of AMPKα at Thr172, as a regulatory node in autophagy induction. Loss- and gain-of-function approaches were utilized to investigate the role of Thr172 in AMPK-mediated autophagy under nutrient stress.
resultsFindings indicated a marked increase in reactive oxygen species-mediated autophagy in hPDLCs under nutrient deprivation. This process was significantly regulated by AMPK activation through Thr172 phosphorylation, establishing AMPK as a critical factor in autophagy induction during cellular adaptation to nutritional stress.
conclusionNutritional stress enhances reactive oxygen species-mediated autophagy in hPDLCs via AMPK signalling, underscoring the role of autophagy in cellular adaptation during OTM. Targeting the AMPK pathway could provide novel insights for optimizing orthodontic treatment by leveraging cellular adaptive mechanisms. CLINICAL RELEVANCE: Understanding the molecular mechanisms underlying autophagy in hPDLCs opens potential therapeutic pathways to improve OTM outcomes. Modulating autophagy may lead to advances in orthodontic therapies that facilitate periodontal tissue remodelling, enhancing clinical effectiveness.
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