ArticleMolecular biology reports2025
Upregulation of TLR-MYD88 signaling, stem cell genes, and Klotho mediates sepsis-associated myocardial inflammation.
Article in Molecular biology reports, 2025. 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.
The trial behind it
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
2 citing papers in PubMed.
- MYD88/TRIF Signaling, Pluripotency and Klotho Regulation in the Intestine, Kidneys, Liver, and Lungs of a Septic Mouse Model.Current issues in molecular biology · 2026Article
- Cardiac Tissue Damage in a Female Animal Post-COVID Model: Relevance of Chemokine-Mediated Inflammation.Viruses · 2025Article
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundSepsis-induced myocardial inflammation involves complex molecular mechanisms that remain incompletely understood.
methodsThis study examined the dynamic temporal expression of critical inflammatory markers, including Toll-like receptors (TLRs), MYD88, Klotho, and stem cell-associated genes (KLF4, HOXA5, NANOG, and HIF1α) within a cecal ligation and puncture-induced murine model of sepsis.
resultsTLR2, TLR3, TLR4, TLR7 and MYD88 exhibited progressive upregulation across 24, 48, and 72 h, highlighting their pivotal role in inflammatory signaling. Klotho expression increased significantly during sepsis, stabilizing at later stages, suggesting a potential modulatory role. Stem cell-associated genes showed dynamic patterns, with KLF4 and NANOG displaying sustained elevation, HOXA5 peaking at 48 h, and HIF1α progressively rising to its highest levels at 72 h.
conclusionsThese findings underscore the interplay between inflammatory pathways and metabolic adaptation in sepsis-induced myocardial injury, potentially providing a foundation for targeted therapeutic strategies.
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40504431What Socratic holds
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.