ArticleClinical and translational medicine2026
Long non-coding RNA lncAPAT promotes atherosclerotic plaque instability by targeting ribosomal protein L22.
Article in Clinical and translational medicine, 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.
- Long non-coding RNA lncAPAT promotes atherosclerotic plaque instability by targeting ribosomal protein L22.Clinical and translational medicine · 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
9 authors.
Funding
Abstract
backgroundLong non-coding RNAs (lncRNAs) regulate macrophage inflammation and atherosclerotic plaque stability, but mechanisms need comprehensive investigations.
methodsWhole-transcriptome sequencing was used to identify a novel human-specific lncRNA, lncAPAT (atherosclerotic plaque instability-associated transcript), in the peripheral blood of patients with coronary artery disease (CAD; n = 5) with mixed plaques on coronary computed tomography angiography (CCTA). LncAPAT was quantified using quantitative real-time polymerase chain reaction in the discovery cohort and independently validated in patients with coronary mixed plaques by CCTA (n = 22) and in patients with acute ST-segment elevation myocardial infarction (STEMI; n = 22). Myeloid cell-specific lncAPAT knock-in mice were generated and injected with recombinant adeno-associated virus of murine proprotein convertase subtilisin/kexin type 9 to induce atherosclerosis and explore the effects of lncAPAT on inflammation and plaque instability. Macrophages were cultured to evaluate lncAPAT function in vitro. Chromatin isolation by RNA purification and sequencing and RNA immunoprecipitation assays were used to identify potential targets of lncAPAT.
resultsLncAPAT expression was highly expressed in the peripheral blood of CAD and STEMI patients compared with the control individuals. Mice with myeloid cell-specific lncAPAT knock-in showed an increased plaque burden (2.7-fold), elevated macrophage counts (2.4-fold), and higher matrix metalloproteinase (MMP) expression (3.3-fold for MMP9, 2.0-fold for MMP2) in thoracic aortic plaques. In vitro, lncAPAT significantly promoted the inflammatory responses, adhesive capacity and cholesterol accumulation of macrophages, and decreased the cholesterol efflux ratio. LncAPAT interacted with the promoter of the ribosomal protein L22 gene (RPL22) and inhibited RPL22 transcription. RPL22 inhibition significantly increased the expression of inflammatory cytokines. The RPL22 protein directly interacted with monocyte chemoattractant protein-1 (MCP-1) mRNA and decreased MCP-1 expression. Furthermore, RPL22 expression in the peripheral blood was lower in CAD and STEMI patients than in control individuals.
conclusionsLncAPAT promoted the macrophage inflammatory response by inhibiting RPL22 transcriptional activity, contributing to plaque instability. KEY POINTS: A novel human-specific long non-coding RNA (lncRNA), named as lncAPAT, is highly expressed in the peripheral blood of patients with coronary mixed plaques. LncAPAT increases thoracic aortic plaque instability and promotes macrophage inflammatory responses. LncAPAT directly interacted with the promoter region of RPL22 to inhibit RPL22 transcriptional activity and increase the expression of MCP-1, thereby contributing to plaque instability.
Indexed as
Identifiers
What 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.