ReviewInflammopharmacology2026
LincRNA-Cox2 at the crossroads of innate immunity and inflammation: mechanisms, disease associations, and therapeutic perspectives.
Review in Inflammopharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Transcriptomic Profiling Reveals Candidate lncRNA-S100-GPCR Co-Expression Networks in Lungs of Piglets Infected withAnimals : an open access journal from MDPI · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
Abstract
Long intergenic non-coding RNA associated with cyclooxygenase-2 (LincRNA-Cox2) has emerged as a prototypical immune-regulatory long non-coding RNA (lncRNA) that integrates pattern-recognition receptor signaling with chromatin remodeling and effector gene transcription in innate immune cells. Originally identified as a highly inducible transcript adjacent to the Ptgs2/Cox2 locus in macrophages, lincRNA-Cox2 displays expression restricted by stimulus and cell type, nuclear localization, and isoform diversity. Mechanistic studies demonstrate that lincRNA-Cox2 exerts both repressive and activating effects on immune-response genes by assembling with heterogeneous nuclear ribonucleoproteins, SWI/SNF complexes, nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), and other signaling intermediates, thereby tuning inflammasome activation, autophagy, Janus kinase/signal transducers and activators of transcription (JAK–STAT) signaling, and cytokine production. Beyond macrophages, lincRNA-Cox2 modulates inflammatory pathways in microglia, dendritic cells, epithelial cells, smooth muscle cells, and other structural cell types, positioning it as a shared regulatory node across tissues. Consistent with these mechanistic roles, altered lincRNA-Cox2 expression has been linked to acute lung injury, chronic smoke-induced airway inflammation, sepsis, bacterial and mycobacterial infections, neuroinflammation, osteoarthritis, metabolic kidney injury, atherosclerosis, pulmonary arterial hypertension, and inflammatory bowel disease. In several of these settings, experimental silencing or pharmacological modulation of lincRNA-Cox2-centered axes ameliorates tissue damage, while clinical studies highlight its potential as a circulating or tissue biomarker. This review synthesizes current knowledge on the biogenesis and molecular actions of lincRNA-Cox2, collates evidence for its involvement in inflammatory, infectious, and malignant disease contexts, and discusses emerging therapeutic and translational opportunities. Together, available data support lincRNA-Cox2 as a context-dependent regulator at the crossroads of innate immunity and inflammation, and as a promising yet complex target for diagnostic and RNA-based therapeutic strategies in human disease.
Indexed as
Identifiers
42020888What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.