ArticleInternational dental journal2026
Lipoteichoic Acid Stimulation of Macrophages Causes Mitochondrial Dysfunction.
Article in International dental journal, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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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.
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Who cites it
2 citing papers in PubMed.
- Fusobacterium nucleatum-Derived Outer Membrane Vesicles Disrupt Epithelial Barrier in Oral Lichen Planus via JNK/c-JUN Mediated Claudin-4 Downregulation.International dental journal · 2026Article
- Immune signaling as a determinant of cellular identity and tissue function.Frontiers in immunology · 2026Review
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Authors and funding
6 authors.
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Abstract
objectivesThis study aimed to investigate the role of mitochondrial dysfunction in the pathogenesis of Enterococcus faecalis and its lipoteichoic acid (LTA)-induced refractory apical periodontitis, and then to evaluate whether the modulation of mitochondrial dynamics with Mdivi-1 could alleviate the ensuing inflammatory response..
methodsAn LTA-induced macrophage model was established to simulate the inflammatory environment of apical periodontitis. Changes in inflammatory factors, mitochondrial morphology, dynamics-related proteins, autophagy markers, and reactive oxygen species (ROS) were analysed. The mitochondrial division inhibitor Mdivi-1 was applied to assess its effects on mitochondrial and inflammatory parameters.
resultsIn the in vivo model, E. faecalis infection successfully induced apical periodontitis, as confirmed by radiographic evidence of periapical bone loss and histological observation of inflammatory cell infiltration. These lesions exhibited a significant upregulation of the pro-inflammatory marker iNOS, concurrently with a downregulation of the mitochondrial protein MFN-2. Consistent with the in vivo findings, LTA stimulation in a cellular model significantly increased the expression of inflammatory mediators (NLRC4, iNOS, NF-κB, Caspase-1) and induced mitochondrial dysfunction, characterised by morphological disruption, dysregulated dynamics, impaired autophagy and elevated ROS levels. Critically, Mdivi-1 treatment mitigated these abnormalities by improving mitochondrial structure and function, normalising dynamics-related protein expression and consequently reducing the inflammatory response.
conclusionsMitochondrial dysfunction plays a central role in LTA-driven inflammatory processes in apical periodontitis. Targeting mitochondrial dynamics with Mdivi-1 can restore mitochondrial function and mitigate macrophage-mediated inflammation, revealing a key mechanism underlying refractory apical periodontitis. CLINICAL SIGNIFICANCE: This study suggests that enhancing mitochondrial function with agents such as Mdivi-1 could serve as a novel therapeutic strategy for refractory apical periodontitis by modulating immune responses and reducing chronic inflammation, potentially improving treatment outcomes in clinically challenging cases.
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