ArticleFundamental research2026
Melatonin ameliorates inflammation-induced mitochondrial dysfunction and cementoblastic differentiation in cells by regulating the METTL3/LINC01444/HSPD1 axis.
Article in Fundamental research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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.
The trial behind it
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Who cites it
1 citing paper in PubMed.
- Progress in Basic Research and Clinical Strategies for Cementum Regeneration.International dental journal · 2025Review
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Authors and funding
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inflammation-induced mitochondrial dysfunction functionally impairs periodontal ligament stem cells (PDLSCs) and hinders their therapeutic efficacy in periodontal regeneration. Melatonin, a mitochondrion-targeted molecule, is considered a promising anti-inflammatory agent in therapeutics, but whether melatonin protects PDLSC cementoblastic differentiation against inflammation-induced damage and the underlying mechanisms of this function remain unclear. This study confirmed that melatonin rescued PDLSC cementoblastic differentiation under inflammatory conditions and that melatonin-induced recovery was linked to ameliorated mitochondrial function in cells. Next, through lncRNA microarray analysis, mass spectrometry and functional studies, an interaction between
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