ArticlePloS one2024
Screening of potential regulatory genes in carotid atherosclerosis vascular immune microenvironment.
Article in PloS one, 2024. 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.
- Single-Cell Analysis, Spatial Transcriptomics and Molecular Docking Unveil Potential Therapeutic Targets for Carotid Atherosclerosis.Balkan medical journal · 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
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundImmune microenvironment is one of the essential characteristics of carotid atherosclerosis (CAS), which cannot be reversed by drug therapy alone. Thus, there is a pressing need to develop novel immunoregulatory strategies to delay this pathological process that drives cardiovascular-related diseases. This study aimed to detect changes in the immune microenvironment of vascular tissues at various stages of carotid atherosclerosis, as well as cluster and stratify vascular tissue samples based on the infiltration levels of immune cell subtypes to distinguish immune phenotypes and identify potential hub genes regulating the immune microenvironment of carotid atherosclerosis. MATERIALS AND
methodsRNA sequencing datasets for CAS vascular tissue and healthy vascular tissue (GSE43292 and GSE28829) were downloaded from the Gene Expression Omnibus (GEO) database. To begin, the immune cell subtype infiltration level of all samples in both GSE43292 and GSE28829 cohorts was assessed using the ssGSEA algorithm. Following this, consensus clustering was performed to stratify CAS samples into different clusters. Finally, hub genes were identified using the maximum neighborhood component algorithm based on the construction of interaction networks, and their diagnostic efficiency was evaluated.
resultsCompared to the controls, a higher number of immune cell subtypes were enriched in CAS samples with higher immune scores in the GSE43292 cohort. Advanced CAS was characterized by high immune cell infiltration, whereas early CAS was characterized by low immune cell infiltration in the GSE28829 cohort. Moreover, CAS progression may be related to the immune response pathway. Biological processes associated with muscle cell development may impede the progression of CAS. Finally, the hub genes PTPRC, ACTN2, ACTC1, LDB3, MYOZ2, and TPM2 had satisfactory efficacy in the diagnosis and prediction of high and low immune cell infiltration in CAS and distinguishing between early and advanced CAS samples.
conclusionThe enrichment of immune cells in vascular tissues is a primary factor driving pathological changes in CAS. Additionally, CAS progression may be related to the immune response pathway. Biological processes linked to muscle cell development may delay the progression of CAS. PTPRC, ACTN2, ACTC1, LDB3, MYOZ2, and TPM2 may regulate the immune microenvironment of CAS and participate in the occurrence and progression of the disease.
Indexed as
Identifiers
What Socratic 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 Socratic graph.