ArticleThe clinical respiratory journal2026
Combined Serum Expression of lncRNA CBR3-AS1 and miR-3163: Prognostic Significance and Underlying Mechanism in Severe Pneumonia.
Article in The clinical respiratory journal, 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
introductionSevere pneumonia (SP) is a life-threatening pulmonary infection characterized by high morbidity, frequent complications, and elevated mortality, with rising global incidence in recent years. This study investigated the prognostic value and molecular mechanisms of lncRNA CBR3-AS1 (CBR3-AS1) in patients with SP.
methodsCBR3-AS1 and miR-3163 levels were evaluated by real-time quantitative polymerase chain reaction (RT-qPCR). The targeting relationship was confirmed by bioinformatics prediction, dual-luciferase activity assay, and RNA immunoprecipitation (RIP) assay. Cell viability and related indicators were detected by cell counting kit-8 (CCK-8), flow cytometry, and enzyme-linked immunosorbent assay (ELISA).
resultsSerum analysis revealed markedly upregulated CBR3-AS1 and downregulated miR-3163 in SP patients versus healthy controls (HC), with bioinformatic and experimental evidence confirming their targeting relationship. In addition, CBR3-AS1 and miR-3163 were influential factors affecting death in SP patients and were sensitive predictors of poor patient prognosis. Mechanistically, silencing CBR3-AS1 promoted the proliferation of MRC-5 cells after LPS induction, although the miR-3163 inhibitor partially abolished these changes. Similarly, oxidative stress and inflammatory markers in MRC-5 cells were also regulated by CBR3-AS1 and miR-3163.
conclusionsCBR3-AS1 sponge miR-3163 mediates MRC-5 cell viability, oxidative stress, and inflammation levels, which ultimately affects the progression of SP. CBR3-AS1/miR-3163 axis represents a promising therapeutic target for improving SP patient outcomes.
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