ArticleHeliyon2024
Melatonin-induced upregulation of telomerase activity interferes with macrophage mitochondrial metabolism and suppresses NLRP3 inflammasome activation in the treatment of Pneumonia.
Article in Heliyon, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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.
The trial behind it
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Who cites it
4 citing papers in PubMed, 4 citations in OpenAlex.
- Therapeutic Potential of Melatonin in Gastrointestinal Cancers: Molecular Mechanisms, Preclinical Evidence and Clinical Implications.Journal of pineal research · 2026Review
- The Impact of Resveratrol and Melatonin on the Genome and Oxidative Status in Ageing Rats.Nutrients · 2025Article
- Toll-like Receptor Activation Remodels the Polyamine and Tryptophan Metabolism in Porcine Macrophages.Metabolites · 2025Article
- Modulating oxidative stress: a reliable strategy for coping with community-acquired pneumonia in older adults.Frontiers in medicine · 2025Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objective: This study aims to investigate the effects of melatonin-induced upregulation of telomerase activity on mitochondrial metabolism and NLRP3 inflammasome activation in macrophages, with the ultimate goal of elucidating potential therapeutic implications for pneumonia treatment. Materials and methods: Macrophages were treated with melatonin to assess its impact on telomerase activity. Mitochondrial function was evaluated through the measurement of reactive oxygen species (ROS) levels and cellular energy production. NLRP3 inflammasome activation was assessed by examining the production of inflammatory cytokines, such as interleukin-1β (IL-1β). The expression levels of key proteins involved in mitochondrial metabolism and NLRP3 inflammasome signaling were also analyzed. Results: Our findings demonstrated that melatonin treatment significantly upregulated telomerase activity in macrophages. This was associated with a reduction in ROS levels and enhanced cellular energy production, indicating improved mitochondrial function. Moreover, melatonin treatment suppressed NLRP3 inflammasome activation, resulting in reduced secretion of IL-1β. The expression levels of proteins involved in mitochondrial metabolism and NLRP3 inflammasome signaling were modulated by melatonin. Conclusion: These results suggest that melatonin-induced upregulation of telomerase activity can interfere with mitochondrial metabolism and inhibit NLRP3 inflammasome activation in macrophages. This indicates a potential therapeutic role for melatonin in the treatment of pneumonia. Understanding the molecular mechanisms underlying these effects may lead to the development of novel therapeutic strategies targeting mitochondria and NLRP3 inflammasome activation for the management of pneumonia. Further investigations are warranted to fully uncover the therapeutic potential of melatonin and its implications for pneumonia treatment.
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Registered trials
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