ArticleInflammation2026
Inhibition of MyD88 in Tubular Epithelial Cells Alleviates the Cellular Senescence in Sepsis-Associated Acute Kidney Injury.
Article in Inflammation, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Cellular senescence has emerged as an important contributor to acute kidney injury (AKI); however, its role in sepsis-associated acute kidney injury (SA-AKI) remains insufficiently characterized. This study aimed to investigate the involvement of cellular senescence in SA-AKI and to determine the contribution of the Toll-like receptor (TLR)/MyD88 signaling pathway. A cecal ligation and puncture (CLP) mouse model was established to induce SA-AKI. Cellular senescence markers and inflammatory indices were evaluated at 24, 48, and 72 h after injury using senescence-associated β-galactosidase (SA-β-Gal) staining, immunofluorescence, and quantitative real-time PCR (qPCR). Integrated transcriptomic and proteomic analyses were performed to identify candidate hub genes involved in SA-AKI. Human Kidney-2 (HK-2) cells were used to assess the role of MyD88 in tubular epithelial cell senescence, and mice with tubular epithelial cell-specific deletion of Myd88 were subsequently used to investigate the in vivo role of MyD88 in SA-AKI. At 72 h after CLP, SA-AKI was associated with a marked increase in SA-β-Gal activity, p21 expression, DNA damage, and inflammatory cytokine production, together with decreased lamin B1 (LAMNB1) expression and reduced proliferative activity, indicating the induction of cellular senescence. Inflammatory cell infiltration was also evident at this time point. Integrated omics analysis identified MyD88 as a key candidate molecule. In HK-2 cells, pharmacological inhibition of MyD88 attenuated lipopolysaccharide-induced cellular senescence and inflammatory responses. Consistently, tubular epithelial cell-specific deletion of Myd88 significantly reduced cellular senescence, inflammatory infiltration, and renal injury following SA-AKI. These findings indicate that cellular senescence in SA-AKI is mediated, at least in part, by the TLR/MyD88 signaling pathway. Targeting this pathway may represent a potential therapeutic strategy for attenuating SA-AKI progression and improving renal outcomes.
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