ArticleCellular & molecular immunology2026
Macrophage CCRL2 promotes NLRP3 inflammasome activation to exacerbate atherosclerosis.
Article in Cellular & molecular immunology, 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.
- Berberine-associated lipid-inflammatory regulation in atherosclerosis: an integrative transcriptomic, single-cell, and in vivo study.Functional & integrative genomics · 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
14 authors.
Funding
Abstract
Atherosclerotic lesions contain heterogeneous macrophage populations with divergent functional phenotypes that play opposing roles in disease progression, creating a major obstacle for the development of macrophage-targeted therapy. The identification of novel molecules that exhibit both preferential expression and functional activity in inflammatory plaque macrophages is crucial for the development of more specific anti-inflammatory therapies against atherosclerosis. Here, we report that the expression of C-C motif chemokine receptor-like 2 (CCRL2), a nonsignaling atypical chemokine receptor initially cloned from LPS-activated macrophages, progressively increased in atherosclerotic lesions during disease progression in both human and mouse models, with predominant expression in inflammatory macrophages characterized by high expression of NLRP3 inflammasome components. Moreover, specific deletion of hematopoietic CCRL2 attenuated atherosclerotic progression in Apoe
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.