ArticleFrontiers in immunology2026
miR-204-5p attenuates inflammatory infiltration in early-stage chronic renal allograft dysfunction by modulating the IL-11/ERK1/2-NF-κB axis.
Article in Frontiers in immunology, 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
Background: Chronic renal allograft dysfunction (CRAD) continues to limit the long-term survival of transplanted kidneys. Inflammatory cell accumulation during the early phase of CRAD may accelerate fibrotic remodeling and graft dysfunction, although the regulatory mechanisms driving this process have not been fully clarified. Interleukin-11 (IL-11) is increasingly recognized as a fibro-inflammatory mediator, but whether miRNA-dependent regulation of IL-11 participates in early CRAD-associated inflammation remains unknown. This study aimed to investigate whether miR-204-5p regulates early inflammatory injury in CRAD by targeting IL-11. Methods and results: A rat CRAD model was established by orthotopic renal transplantation, and kidney tissues were collected at 12 weeks post-transplantation to assess early inflammatory and fibrotic changes. IL-11 expression was inhibited Conclusion: miR-204-5p attenuates early inflammatory injury in CRAD by directly targeting IL-11 and suppressing IL-11-associated ERK1/2-NF-κB inflammatory signaling. The miR-204-5p/IL-11 axis may represent a potential regulatory pathway and therapeutic target for early inflammatory injury in CRAD.
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