Evidence map›Paper›PMID 39849527›Full record

ArticleJournal of translational medicine2025

From bench to bedside: elucidating VEGF(R) inhibitor-related heart failure in cancer treatment.

Shengkun Peng, MinHong Cai, Hongyu Kuang, Anqi Lin, Qinghua Ma, Xiaoqin Dai, Peng Luo, Yijun Liu, Guo Zhang, Yifeng Bai

Abstract read
In one paragraph

Article in Journal of translational medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed, 1 pooled it
–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

4 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Cu(OH)Particle and fibre toxicology · 2026
    Article
  3. Article
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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

10 authors.

Shengkun Peng *Department of Radiology, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu, 610072, Sichuan, China.
MinHong Cai *Healthcare-Associated Infection Management Office, Sichuan Academy of Medical Sciences and Sichuan People's Hospital, Chengdu, Sichuan, China.
Hongyu Kuang *Department of Cardiology, University-town Hospital of Chongqing Medical University, Chongqing, China.
Anqi Lin *Department of Oncology, Zhujiang Hospital, Southern Medical University, Guangzhou, China.
Qinghua MaDepartment of Pediatrics, Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, China.
Xiaoqin DaiDepartment of Traditional Chinese Medicine, Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, China.
Peng LuoDepartment of Oncology, Zhujiang Hospital, Southern Medical University, Guangzhou, China. luopeng@smu.edu.cn.
Yijun LiuDepartment of Outpatient, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu, China. 36547480@qq.com.
Guo ZhangDepartment of Dean's office, Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, China. 1949618@qq.com.
Yifeng BaiDepartment of Oncology, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu, China. baiyifeng@med.uestc.edu.cn.ORCID 0000-0002-5595-3963

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundVascular endothelial growth factor (VEGF) and VEGF receptor (VEGFR) inhibitors play a pivotal role in treating various tumors; however, the clinical characteristics and molecular mechanisms of their associated heart failure (HF) remain incompletely understood.

methodsWe investigated the epidemiological characteristics of VEGF or VEGFR inhibitors [VEGF(R)i]-related heart failure (VirHF) using the global pharmacovigilance database Vigibase. The phenotypic features and molecular mechanisms of VirHF were characterized using VEGF(R)i-treated mouse models through a combination of echocardiography, histopathological analysis, and transcriptome sequencing. Furthermore, we performed a retrospective analysis of cardiac function parameters in patients undergoing VEGF(R)i treatment at local hospitals.

resultsIn the analysis of 1871 VirHF cases, elderly patients (≥ 65 years) and female subjects demonstrated an elevated risk of occurrence. Experimental studies in mice revealed that both acute and chronic VEGF(R)i administration resulted in reduced left ventricular EF, cardiomyocyte hypertrophy, and myocardial fibrosis. Transcriptomic analysis identified significant dysregulation of multiple key signaling pathways, including DNA repair (R = 0.46), mitochondrial ATP synthesis (R = 0.39), glycogen metabolism regulation (R = 0.45), and proteasome-mediated protein degradation (R = 0.45). Moreover, significant upregulation was observed in inflammatory pathways, specifically those involving IL-1, IL-6, TNF-α, and IRF3/IRF7-mediated immune responses. Clinical cohort analyses demonstrated significant elevations in both cardiac injury biomarkers (NT-proBNP, CK-MB, cTnT) and inflammatory mediators (CRP) following VEGF(R)i administration.

conclusionsOur findings present the first comprehensive characterization of VirHF clinical features and elucidate its underlying molecular mechanisms, thereby providing a theoretical framework for optimizing the clinical safety of VEGF(R)i therapy.

Indexed as

Heart FailureNeoplasmsReceptors, Vascular Endothelial Growth FactorTranslational Research, BiomedicalAgedAnimalsFemaleHumansMaleMiceSignal TransductionVascular Endothelial Growth Factor AReceptors, Vascular Endothelial Growth FactorVascular Endothelial Growth Factor AMouse modelVascular endothelial growth factorVascular endothelial growth factor receptorVEGF(R) inhibitor-related heart failureVigiBase

Identifiers

PMID39849527
PMCPMC11756202

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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.