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pmid:40269003

CDC6 as early biomarker for myocardial infarction with acute cellular senescence and repair mechanisms.

Yun Wen · Xiaofang Zhang · Jiaxin Wang · Caixia Ma · Liangyan Wu · Lihong Wang

Scientific reports · 2025 doi:10.1038/s41598-025-94988-x

Paper

complete

Experiment

complete

Data

partial

Analysis

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absent

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pmid:40269003
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title
CDC6 as early biomarker for myocardial infarction with acute cellular senescence and repair mechanisms.
doi
10.1038/s41598-025-94988-x
pmid
40269003
authors array · 6 items
[0]
Yun Wen
[1]
Xiaofang Zhang
[2]
Jiaxin Wang
[3]
Caixia Ma
[4]
Liangyan Wu
[5]
Lihong Wang
journal
Scientific reports
year
2025
abstract
We aimed to the exploration of genes related to the cell cycle and the mechanisms of cardiac cell repair and senescence post-MI. The sequencing dataset of myocardial infarction in mice (GSE161427) was downloaded from the Gene Expression Omnibus (GEO) database, yielding 894 upregulated differentially expressed genes (DEGsup). Additionally, 494 senescence-related genes (SRGs) were obtained from the CellAge database. The overlapping differentially expressed genes (DEupSGs) between these two sets were identified using the R software. WGCNA using the GSE59867 dataset revealed a highly related module to MI. The intersection of core genes from the purple module and DEupSGs yielded 12 genes. Through machine learning and PPI analysis, two target genes related to MI and cellular senescence were identified: CDC6 and PLK1. ROC curve analysis using the MI animal myocardial sample dataset GSE775 and the patient blood sample dataset GSE60993 indicated that CDC6 expression has high diagnostic value for MI and cellular senescence, with differential expression levels at various times post-infarction.These results show that CDC6 is specifically upregulated in the early stages of MI, and both in vivo and ex vivo model results are consistent with bioinformatics findings. Additionally, overexpression of CDC6 in the early oxygen-glucose deprivation (OGD) model in vitro increased the expression of genes mediating cardiac repair. Interestingly, when ABT263 was used to clear senescent cells, the expression of genes mediating repair in primary cardiac cells decreased, suggesting that acute ischemic hypoxia early on, CDC6-mediated acute cardiac cell senescence may promote early cardiac repair. This finding may provide new insights into the monitoring and assessment of cardiac cell senescence and repair in the early stages of MI.
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The 2 target genes was further validated using ROC curve analysis with external validation sets GSE775 and GSE60993, employing the pROC package in R to calculate the area under the curve (AUC).
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sections[8] "Identification of the core target gene CDC6" paragraph 2
quote
The 2 target genes was further validated using ROC curve analysis with external validation sets GSE775 and GSE60993, employing the pROC package in R to calculate the area under the curve (AUC).
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The raw data of the four microarray datasets (accession numbers GSE161427, GSE59867, GSE775 and GSE60993)were downloaded from the GEO repository (https://www.ncbi.nlm.nih.gov/geo/). All data are publicly accessible.
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sections[25] "notes" paragraph 1
quote
The raw data of the four microarray datasets (accession numbers GSE161427, GSE59867, GSE775 and GSE60993)were downloaded from the GEO repository (https://www.ncbi.nlm.nih.gov/geo/). All data are publicly accessible.
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Among the 2 target genes, only the gene CDC6 showed an area under the curve (AUC) > 0.7 in both datasets (Fig. 6A–D).
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sections[18] "Evaluation of the diagnostic efficacy of post-MI senescence-related core target genes" paragraph 3
quote
Among the 2 target genes, only the gene CDC6 showed an area under the curve (AUC) > 0.7 in both datasets (Fig. 6A–D).
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Among the 2 target genes, only the gene CDC6 showed an area under the curve (AUC) > 0.7 in both datasets (Fig. 6A–D).
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The raw data of the four microarray datasets (accession numbers GSE161427, GSE59867, GSE775 and GSE60993)were downloaded from the GEO repository (https://www.ncbi.nlm.nih.gov/geo/). All data are publicly accessible.
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[435]
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6244
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Homo sapiens
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Gene expression profiling reveals potential prognostic biomarkers associated with the progression of heart failure
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2026-11-01T15:39:54Z
resolution_check
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[3] object · 15 fields
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data:geo:GSE60993
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The raw data of the four microarray datasets (accession numbers GSE161427, GSE59867, GSE775 and GSE60993)were downloaded from the GEO repository (https://www.ncbi.nlm.nih.gov/geo/). All data are publicly accessible.
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GEO
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GEO accession URL
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The raw data of the four microarray datasets (accession numbers GSE161427, GSE59867, GSE775 and GSE60993)were downloaded from the GEO repository (https://www.ncbi.nlm.nih.gov/geo/). All data are publicly accessible.
access_statement_kind
data_availability_statement
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[32]
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33
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null
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null
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6884
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Homo sapiens
title
Assessment and Diagnostic Relevance of Novel Serum Biomarkers for Early Decision of ST-elevation Myocardial Infarction
resolution_checked_at
2026-11-01T15:39:55Z
resolution_check
identifier_resolution_only_no_download_no_licence_read
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false
licence_read
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data:geo:GSE775
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https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE775
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null
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The raw data of the four microarray datasets (accession numbers GSE161427, GSE59867, GSE775 and GSE60993)were downloaded from the GEO repository (https://www.ncbi.nlm.nih.gov/geo/). All data are publicly accessible.
structure object · 15 fields
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GEO
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GEO accession URL
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The raw data of the four microarray datasets (accession numbers GSE161427, GSE59867, GSE775 and GSE60993)were downloaded from the GEO repository (https://www.ncbi.nlm.nih.gov/geo/). All data are publicly accessible.
access_statement_kind
data_availability_statement
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GSM12380
sample_count
59
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null
group_sizes_basis
null
platform
81
taxon
Mus musculus
title
Mouse model of myocardial infarction
resolution_checked_at
2026-11-01T15:39:55Z
resolution_check
identifier_resolution_only_no_download_no_licence_read
downloaded
false
licence_read
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gaps array · 8 items
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[5]
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asset:data:geo:GSE775 licence not read
analysis object · 4 fields
state
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id
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diagnostic_evaluation
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reference_standard_and_test
evidence object · 3 fields
score
1
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The 2 target genes was further validated using ROC curve analysis with external validation sets GSE775 and GSE60993, employing the pROC package in R to calculate the area under the curve (AUC).
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method-2
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group_comparison
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group_summary
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welch_t
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two_or_more_groups_continuous
evidence object · 3 fields
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analysis of variance
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differential_expression
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Differential expression analysis
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normalise_counts
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evidence object · 3 fields
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limma
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build_graph
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evidence object · 3 fields
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method.reader_differs_from_extractor
capability object · 3 fields
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complete
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capability_id
capability:computational_analysis
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Computational analysis platform
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meta_analysis
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candidate
Automated Assays Laravel application and simulated adapters
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readiness object · 8 fields
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nothing:replicable_now
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confusion_counts
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basis
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tier
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capability:computational_analysis
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owned
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data object · 6 fields
tier
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basis
The paper names GSE161427, GSE59867, GSE775, GSE60993 in Gene Expression Omnibus (GEO) database and the accession resolves in the repository. No dataset was downloaded and no licence was read.
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source:pmid:40269003
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data:geo:GSE161427
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extraction_review
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minimax
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minimax
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pmid:40269003
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paper
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source:pmid:40269003
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manuscript
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PMID 40269003 full text
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data:geo:GSE161427
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GEO GSE161427
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egulated in the early stages of MI, and both in vivo and ex vivo model results are consistent wit
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sequencing dataset of myocardial infarction in mice (GSE161427) was downloaded from the Gene Exp
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The 2 target genes was further validated using ROC curve analysis with external validation sets GSE775 and GSE60993, employing the pROC package in R to calculate the area under the curve (AUC).
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{"sci_version": "1.2", "schema": "https://corpus.bntrg.co.uk/sci/1.0/sci.schema.json", "id": "pmid:40269003", "kind": "science-record", "revision": 4, "content_hash": "sha256:b75ecdebbd8909f3ef5dc1148c6bdc2b76cc978ba76bf89ec04c1f53ccf4d329", "created_at": "2026-11-01T20:30:25Z", "updated_at": "2026-11-01T22:56:24Z", "generator": {"name": "corpus-assay-engine", "run_id": "reading-sci-2026-11-01"}, "paper": {"state": "complete", "title": "CDC6 as early biomarker for myocardial infarction with acute cellular senescence and repair mechanisms.", "doi": "10.1038/s41598-025-94988-x", "pmid": "40269003", "authors": ["Yun Wen", "Xiaofang Zhang", "Jiaxin Wang", "Caixia Ma", "Liangyan Wu", "Lihong Wang"], "journal": "Scientific reports", "year": 2025, "abstract": "We aimed to the exploration of genes related to the cell cycle and the mechanisms of cardiac cell repair and senescence post-MI. The sequencing dataset of myocardial infarction in mice (GSE161427) was downloaded from the Gene Expression Omnibus (GEO) database, yielding 894 upregulated differentially expressed genes (DEGsup). Additionally, 494 senescence-related genes (SRGs) were obtained from the CellAge database. The overlapping differentially expressed genes (DEupSGs) between these two sets were identified using the R software. WGCNA using the GSE59867 dataset revealed a highly related module to MI. The intersection of core genes from the purple module and DEupSGs yielded 12 genes. Through machine learning and PPI analysis, two target genes related to MI and cellular senescence were identified: CDC6 and PLK1. ROC curve analysis using the MI animal myocardial sample dataset GSE775 and the patient blood sample dataset GSE60993 indicated that CDC6 expression has high diagnostic value for MI and cellular senescence, with differential expression levels at various times post-infarction.These results show that CDC6 is specifically upregulated in the early stages of MI, and both in vivo and ex vivo model results are consistent with bioinformatics findings. Additionally, overexpression of CDC6 in the early oxygen-glucose deprivation (OGD) model in vitro increased the expression of genes mediating cardiac repair. Interestingly, when ABT263 was used to clear senescent cells, the expression of genes mediating repair in primary cardiac cells decreased, suggesting that acute ischemic hypoxia early on, CDC6-mediated acute cardiac cell senescence may promote early cardiac repair. 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