ArticleClinical epigenetics2026
CCR1 as a potential regulator of neutrophil-mediated pathogenesis in post-acute ischemic stroke: a multi-omics Mendelian randomization.
Article in Clinical epigenetics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
Abstract
backgroundThe genetic and immunological mechanisms underlying post-acute ischemic stroke (IS) remain incompletely understood, particularly those involving neutrophil-mediated inflammation. This study aimed to identify genes associated with IS using a multi-omics Mendelian randomization framework.
methodsSummary-data-based Mendelian Randomization (SMR) was used to identify upstream genetic regulators of neutrophil-driven pathogenesis. We systematically screened 949 neutrophil-related genes using SMR analyses across multi-omics quantitative trait loci (QTL) datasets (methylation, expression, and protein). We then validated temporal expression patterns in independent IS cohorts and constructed a diagnostic nomogram to assess clinical discrimination.
resultsMulti-omics SMR analysis identified CCR1, DEFA4, SH2B3 and CDKN1A as potential genes associated with IS risk. In independent clinical validation cohorts, CCR1 and DEFA4 were consistently upregulated in the peripheral blood of IS patients. Notably, CCR1 emerged as a central hub gene; its expression exhibited a potential association with neutrophil abundance (R = 0.31) and functional hyperactivation pathways, including chemotaxis and cytotoxicity. Furthermore, a diagnostic nomogram integrating CCR1 and DEFA4 demonstrated high discriminatory power (AUC = 0.875), underscoring their potential as precision biomarkers.
conclusionsIdentified as a potential neutrophil-related genetic factor, CCR1 is associated with ischemic injury and may contribute to neutrophil chemotaxis and functional hyperactivation. Consequently, targeting CCR1 offers a precision therapeutic strategy to attenuate neuroinflammation.
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.