Molecular biology reports · 2025
Upregulation of TLR-MYD88 signaling, stem cell genes, and Klotho mediates sepsis-associated myocardial inflammation.
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Mylonas Konstantinos S, Peroulis Michail, Schizas Dimitrios, Boletis John N, Kapelouzou Alkistis
Аннотация
BACKGROUND: Sepsis-induced myocardial inflammation involves complex molecular mechanisms that remain incompletely understood.
METHODS: This 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.
RESULTS: TLR2, 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.
CONCLUSIONS: These findings underscore the interplay between inflammatory pathways and metabolic adaptation in sepsis-induced myocardial injury, potentially providing a foundation for targeted therapeutic strategies.
METHODS: This 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.
RESULTS: TLR2, 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.
CONCLUSIONS: These findings underscore the interplay between inflammatory pathways and metabolic adaptation in sepsis-induced myocardial injury, potentially providing a foundation for targeted therapeutic strategies.
Предметные рубрики MeSH
AnimalsMyeloid Differentiation Factor 88SepsisKlotho ProteinsSignal TransductionMiceKruppel-Like Factor 4GlucuronidaseToll-Like ReceptorsUp-RegulationMaleInflammationDisease Models, AnimalMyocarditisStem CellsMice, Inbred C57BLKruppel-Like Transcription FactorsHypoxia-Inducible Factor 1, alpha SubunitMyocardium