Evidence map›Paper›PMID 41239464›Full record

ArticleCell division2025

Integrating genetic crosstalk between atherosclerosis and lung adenocarcinoma to advance precision diagnosis and treatment.

Haojie Dai, Xuchen Wang, Qiwen Wu, Ye Tan, Haoran Shen, Yichun Gu, Chuanxin Su, Aidong Chen

Abstract read
In one paragraph

Article in Cell division, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

29 citing papers in PubMed.

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  5. Decoding chromatin regulator-LAIR1Clinical and experimental medicine · 2026
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors.

Haojie Dai *The Key Laboratory of Targeted Intervention of Cardiovascular Disease, Collaborative Innovation Center for Cardiovascular Disease Translational Medicine, Department of Physiology, Nanjing Medical University, Nanjing, 211166, Jiangsu, China.
Xuchen Wang *The Key Laboratory of Targeted Intervention of Cardiovascular Disease, Collaborative Innovation Center for Cardiovascular Disease Translational Medicine, Department of Physiology, Nanjing Medical University, Nanjing, 211166, Jiangsu, China.
Qiwen WuDepartment of Laboratory Medicine, The First Affiliated Hospital of Wannan Medical College, Wuhu, 241001, China.
Ye TanThe Key Laboratory of Targeted Intervention of Cardiovascular Disease, Collaborative Innovation Center for Cardiovascular Disease Translational Medicine, Department of Physiology, Nanjing Medical University, Nanjing, 211166, Jiangsu, China.
Haoran ShenThe Key Laboratory of Targeted Intervention of Cardiovascular Disease, Collaborative Innovation Center for Cardiovascular Disease Translational Medicine, Department of Physiology, Nanjing Medical University, Nanjing, 211166, Jiangsu, China.
Yichun GuThe Key Laboratory of Targeted Intervention of Cardiovascular Disease, Collaborative Innovation Center for Cardiovascular Disease Translational Medicine, Department of Physiology, Nanjing Medical University, Nanjing, 211166, Jiangsu, China.
Chuanxin SuDepartment of Immunology, School of Cell and Gene Therapy, Songjiang Research Institute, Songjiang Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China. pd365429@shsmu.edu.cn.
Aidong ChenThe Key Laboratory of Targeted Intervention of Cardiovascular Disease, Collaborative Innovation Center for Cardiovascular Disease Translational Medicine, Department of Physiology, Nanjing Medical University, Nanjing, 211166, Jiangsu, China. aidongchen@njmu.edu.cn.

Funding

the National Natural Science Foundation of China 31571168
6 · The paper itself

Abstract

There is evidence that atherosclerosis is a "tumor-like" disease and has similar genetic mutations to lung adenocarcinoma. In addition, the treatment and progression of lung adenocarcinoma can contribute to the development of atherosclerosis. This highlights the importance of studying the mechanisms of crosstalk between these two diseases and developing tools for early diagnosis and prognosis. We obtained gene expression profiles of both diseases through the GEO and TCGA databases and screened for crosstalk genes on the basis of differential genes. On the one hand, we constructed a diagnostic model of AS with LUAD by screening the core genes through Lasso and SVM-RFE to advance the early diagnosis of AS in patients with LUAD and explored the association between the core genes and immune infiltration. On the other hand, we constructed a robust prognostic model of LUAD based on crosstalk genes, explored the potential mechanisms of prognostic model genes in the regulation of immune infiltration and predicted treatment differences in LUAD patients to advance clinical decision-making. In addition, we constructed a PPI network based on crosstalk genes and a TF-miRNA-mRNA network, and performed drug prediction and molecular docking validation based on core targets. In conclusion, we revealed the crosstalk between AS and LUAD based on multifaceted transcriptomic analysis, screened novel targets, advanced diagnosis and prognosis, explored potential drugs and treatments, and provided invaluable insights into the research and treatment of AS with LUAD.

Indexed as

AtherosclerosisBiomarkerCrosstalkDiagnosisLung adenocarcinomaPrognosis

Identifiers

PMID41239464
PMCPMC12619290

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

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.