Evidence map›Paper›PMID 41905182›Full record

ArticleRedox biology2026

Systolic pressure overload caused pulmonary oxidative stress, vessel remodeling and severe microvascular thrombosis in CD40 knockout mice through promoting platelet aggregation.

Wenhui Yue, Yanyan Xu, Xinyu Weng, Dongzhi Wang, Linlin Shang, Haojie Jiang, Edward Kenneth Weir, Junling Liu, Yawei Xu, Wenliang Che and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Redox biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

11 authors.

Wenhui YueDepartment of Cardiology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai, 200072, China. Electronic address: yuewenhui3@163.com.
Yanyan XuRuijin Hospital, Department of Laboratory Medicine, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, China; College of Health Sciences and Technology, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai jiao Tong University School of Medicine, Shanghai, 200025, China.
Xinyu WengDepartment of Cardiology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai, 200072, China; Department of Cardiology, Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital, Fudan University, Shanghai, 200025, China; Lillehei Heart Institute and Department of Medicine, University of Minnesota Medical School, Minneapolis, MN, 55455, USA.
Dongzhi WangDepartment of Cardiology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai, 200072, China; Department of Physiology & Biophysics, University of Mississippi Medical Center, Jackson, MS, 39216, USA.
Linlin ShangDepartment of Cardiology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai, 200072, China.
Haojie JiangDepartment of Biochemistry and Molecular Cell Biology, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, China.
Edward Kenneth WeirLillehei Heart Institute and Department of Medicine, University of Minnesota Medical School, Minneapolis, MN, 55455, USA.
Junling LiuDepartment of Biochemistry and Molecular Cell Biology, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, China.
Yawei XuDepartment of Cardiology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai, 200072, China.
Wenliang CheDepartment of Cardiology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai, 200072, China. Electronic address: chewenliang@tongji.edu.cn.
Yingjie ChenDepartment of Physiology & Biophysics, University of Mississippi Medical Center, Jackson, MS, 39216, USA. Electronic address: ychen2@umc.edu.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pulmonary thrombosis is a fatal complication observed in patients following severe trauma or pulmonary infections. Patients with existing heart failure (HF) are more susceptible to infection-induced lung thrombosis; however, the underlying mechanisms remain poorly understood. This study introduces a severe mouse pulmonary thrombosis model utilizing CD40 knockout (KO) mice following transverse aortic constriction (TAC)-induced HF. While CD40 KO was found to have no detectable effect on left ventricular (LV) structure or function in mice either after TAC or under control conditions, the CD40 KO mice developed profound pulmonary micro-thrombosis after TAC. CD40 deficiency also significantly exacerbated TAC-induced pulmonary leukocyte infiltration (such as total CD45

Indexed as

CD40 AntigensOxidative StressPlatelet AggregationThrombosisVascular RemodelingAnimalsDisease Models, AnimalLungMaleMiceMice, KnockoutVascular Cell Adhesion Molecule-1CD40 AntigensVascular Cell Adhesion Molecule-1Heart failureInflammationPlatelet dysfunctionPulmonary thrombosis

Identifiers

PMID41905182
PMCPMC13054292

What Socratic holds

Textmetadata
LicenceCC BY
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.