Evidence map›Paper›PMID 40568844›Full record

ArticleAutophagy2025

Excessive autophagic degradation of MYLK3 causes sunitinib-induced cardiotoxicity.

Ziwei Pan, Lujie Zhu, Xiaochen Wang, Ning Huangfu, Pengpeng Su, Fangkun Yang, Xuyang Fu, Linbin Pu, Qiuli Fu, Jinghai Chen and 3 more

Abstract read
In one paragraph

Article in Autophagy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Review
  2. Article
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

13 authors.

Ziwei PanDepartment of Cardiology, The First Affiliated Hospital of Ningbo University, Ningbo, China.
Lujie ZhuDepartment of Cardiology, The First Affiliated Hospital of Ningbo University, Ningbo, China.
Xiaochen WangKey Laboratory of combined Multi-organ Transplantation, Ministry of Public Health, the First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Ning HuangfuDepartment of Cardiology, The First Affiliated Hospital of Ningbo University, Ningbo, China.
Pengpeng SuDepartment of Cardiology, The First Affiliated Hospital of Ningbo University, Ningbo, China.
Fangkun YangDepartment of Cardiology, The First Affiliated Hospital of Ningbo University, Ningbo, China.
Xuyang FuInstitute of Translational Medicine, Zhejiang University, Hangzhou, China.
Linbin PuInstitute of Translational Medicine, Zhejiang University, Hangzhou, China.
Qiuli FuEye Center of the Second Affiliated Hospital, and Zhejiang Provincial Key Lab of Ophthalmology, Zhejiang University School of Medicine, Hangzhou, China.
Jinghai ChenInstitute of Translational Medicine, Zhejiang University, Hangzhou, China.
Hanbin CuiDepartment of Cardiology, The First Affiliated Hospital of Ningbo University, Ningbo, China.
Ping LiangKey Laboratory of combined Multi-organ Transplantation, Ministry of Public Health, the First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.ORCID 0000-0001-6806-3735
Jiaxi ShenDepartment of Cardiology, The First Affiliated Hospital of Ningbo University, Ningbo, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sunitinib is a receptor tyrosine kinase inhibitor used for the treatment of renal cell carcinoma and imatinib-resistant gastrointestinal stromal tumors. Clinical data have shown that patients receiving sunitinib develop reduced cardiac function, arrhythmia and heart failure, thereby largely limiting its clinical use. However, the molecular mechanisms underlying sunitinib-induced arrhythmogenesis remain unclear. Here, utilizing the human induced pluripotent stem cell-derived cardiomyocyte (iPSC-CM) model, we found that sunitinib caused a variety of deleterious phenotypes, including cardiomyocyte death, sarcomeric disorganization, irregular Ca

Indexed as

AutophagyCardiotoxicityProtein Serine-Threonine KinasesSunitinibAnimalsArrhythmias, CardiacCalciumCalcium-Calmodulin-Dependent Protein Kinase Type 2HumansInduced Pluripotent Stem CellsMiceMyocytes, CardiacProteolysisSarcoplasmic Reticulum Calcium-Transporting ATPasesSequestosome-1 ProteinCalciumCalcium-Calmodulin-Dependent Protein Kinase Type 2Protein Serine-Threonine KinasesSarcoplasmic Reticulum Calcium-Transporting ATPasesSequestosome-1 ProteinSunitinibArrhythmiaautophagyiPSC-derived cardiomyocytesMYLK3sunitinib-induced cardiotoxicity

Identifiers

PMID40568844
PMCPMC12758171

What OpenQuestion holds

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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 OpenQuestion graph.