Evidence map›Paper›PMID 41074588›Full record

ArticleActa biochimica et biophysica Sinica2025

Carfilzomib triggers cardiotoxicity by suppressing SENP1-mediated deSUMOylation of DDX17.

Sheng Wang, Jingjing Wang, Xin Li, Zhigao Dai, Tiantian Li, Yixuan Wang, Ziyi Peng, Mengqi Wang, Hao Cheng, Linchuang Jia and 7 more

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In one paragraph

Article in Acta biochimica et biophysica Sinica, 2025. 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
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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

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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

17 authors.

Sheng WangDepartment of Pathophysiology, School of Basic Medical Science, Tianjin Medical University, Tianjin 300070, China.
Jingjing WangShandong Provincial Key Laboratory of Precision Oncology, Shandong Cancer Hospital and Institute, Shandong First Medical University and Shandong Academy of Medical Sciences, Jinan 250117, China.
Xin LiHouston Methodist Cancer Center, Weill Cornell Medicine, Houston, TX 77030, USA.
Zhigao DaiDepartment of Cardiology, Hebei Port Group Qinhuangdao Hospital of Integrated Traditional Chinese and Western Medicine, Qinhuangdao 066000, China.
Tiantian LiDepartment of Pathophysiology, School of Basic Medical Science, Tianjin Medical University, Tianjin 300070, China.
Yixuan WangDepartment of Pathophysiology, School of Basic Medical Science, Tianjin Medical University, Tianjin 300070, China.
Ziyi PengDepartment of Pathophysiology, School of Basic Medical Science, Tianjin Medical University, Tianjin 300070, China.
Mengqi WangDepartment of Pathophysiology, School of Basic Medical Science, Tianjin Medical University, Tianjin 300070, China.
Hao ChengDepartment of Pathophysiology, School of Basic Medical Science, Tianjin Medical University, Tianjin 300070, China.
Linchuang JiaDepartment of Pathophysiology, School of Basic Medical Science, Tianjin Medical University, Tianjin 300070, China.
Danchen SuDepartment of Pathophysiology, School of Basic Medical Science, Tianjin Medical University, Tianjin 300070, China.
Mu QiaoDepartment of Pathophysiology, School of Basic Medical Science, Tianjin Medical University, Tianjin 300070, China.
Jingya WangDepartment of Pathophysiology, School of Basic Medical Science, Tianjin Medical University, Tianjin 300070, China.
Ying XieShandong Provincial Key Laboratory of Precision Oncology, Shandong Cancer Hospital and Institute, Shandong First Medical University and Shandong Academy of Medical Sciences, Jinan 250117, China.
Jing GuoShandong Provincial Key Laboratory of Precision Oncology, Shandong Cancer Hospital and Institute, Shandong First Medical University and Shandong Academy of Medical Sciences, Jinan 250117, China.
Xiaozhi LiuTianjin Key Laboratory of Epigenetics for Organ Development of Preterm Infants, Tianjin Fifth Central Hospital, Tianjin 300450, China.
Tong LiuTianjin Key Laboratory of Ionic-Molecular Function of Cardiovascular Disease, Department of Cardiology, Tianjin Institute of Cardiology, Second Hospital of Tianjin Medical University, Tianjin 300211, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Carfilzomib (Cfz) is a second-generation proteasome inhibitor approved for the treatment of relapsed/refractory multiple myeloma (RRMM). Previous studies have shown that Cfz is associated with a higher incidence of severe adverse cardiac effects than bortezomib (Btz); however, the underlying mechanisms remain to be elucidated. The aim of this study is to identify key regulators of cardiotoxicity induced by Cfz and to investigate the mechanisms by which these factors exert their effects. We establish a mouse model of cardiac toxicity induced by Cfz and confirm the phenotype through cardiac functional analysis, morphology assessment, myocardial fibrosis, and apoptosis analysis. We subsequently perform RNA sequencing to identify differentially expressed genes (DEGs) and further validate their functions and mechanisms. We find that Cfz induces myocardial hypertrophy and myocardial injury, along with the suppression of SENP1 expression in mouse heart tissues and

Indexed as

CardiotoxicityCysteine EndopeptidasesDEAD-box RNA HelicasesEndopeptidasesOligopeptidesSumoylationAnimalsApoptosisHumansMaleMiceMice, Inbred C57BLMyocytes, CardiacRatscarfilzomibCysteine EndopeptidasesDEAD-box RNA HelicasesEndopeptidasesOligopeptidesSenp1 protein, mousecardio-oncologycarfilzomibDDX17SENP1SUMOylation

Identifiers

PMID41074588
PMCPMC13449089

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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.