ArticleHeliyon2025
The potential of melatonin in sepsis-associated acute kidney injury: Mitochondrial protection and cGAS-STING signaling pathway.
Article in Heliyon, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
7 citing papers in PubMed.
- [Melatonin alleviates cardiomyocyte necroptosis in diabetic mice by inhibiting the STING signaling pathway].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026Article
- Crosstalk between innate immune signaling pathways and integrated TLR, NLRP3 inflammasome, cGAS-STING, and NF-κB networks in sepsis.Frontiers in cell and developmental biology · 2026Review
- Melatonin Administration Attenuates High-Fat-Diet-Induced Renal Damage in Wistar Rats.Biomolecules · 2025Article
- Article
- Updated insights on ASK1 signaling: mechanisms, regulation, and therapeutic potential in diseases.Molecular and cellular biochemistry · 2025Review
- Neuropsychiatric symptoms in the context of hemodynamic disruption during septic shock.World journal of psychiatry · 2025Article
- Article
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Melatonin (Mel) is known for various biological function, such as antioxidant and anti-inflammatory capabilities, as well as its ability to modulate immune responses, which can protect mitochondria and improve the prognosis of sepsis-associated acute kidney injury (SA-AKI). However, there is a multitude of theories regarding how Mel exerts its immune-modulating functions, with no consensus reached as of yet. We propose the protective effects of Mel on mitochondria are closely related to the cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) signaling pathway in the immune-inflammatory response. We intraperitoneally injected H151 and Mel into SA-AKI mouse models to interfere the cGAS-STING signaling pathway. By comparing behavioral, pathological, and molecular biology results, we discovered that Mel could reduce cGAS-STING signaling pathway while greatly relieving kidney damage and function. In addition, Mel-treated mice showed a significant increase in autophagosome formations, which might be linked to the cGAS-STING signaling pathway. Our findings suggest that Mel protection on kidney injury in SA-AKI mice is partially attributed to the inhibition of the cGAS-STING signaling pathway.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.