ArticleFrontiers in immunology2025
Regulation of ZFP36 by lncOlfr29 promotes inflammation through NLRP3.
Article in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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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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Who cites it
2 citing papers in PubMed.
- Sleep Deprivation and Neuronal Hyperexcitation Share Transcriptomic Signatures.Neuropsychopharmacology reports · 2026Article
- The ZFP36 Family as Post-Transcriptional Regulators in Physiology and Disease.International journal of molecular sciences · 2026Review
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Authors and funding
5 authors.
Funding
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Abstract
Objective: The functional state of macrophages is regulated by multiple factors and closely related to the occurrence and development of various diseases. The aim of this study is to discover a new regulatory factor in macrophages, which can serve as a target for disease prevention and treatment. Methods: Long non-coding RNA (lncRNA) lncOlfr29 was discovered through RNA sequencing. The functions of lncOlfr29 were investigated by bioinformatics analysis, lncOlfr29 shRNA silencing and overexpressing adenovirus, and lncOlfr29 knockout (KO) mice. To investigate the function of lncOlfr29 Results: We here identified a novel lncRNA named lncOlfr29 in macrophages and demonstrated that lncOlfr29 promoted inflammation by enhancing NLRP3-mediated IL-1 β maturation and pyroptosis of macrophages. Conclusion: Our data demonstrate that lncOlfr29 can regulate expression of NLRP3 through binding with ZFP36. These results will provide new insights into the treatment of inflammatory diseases.
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