Evidence map›Paper›PMID 40389799›Full record

ArticleCardiovascular toxicology2025

ELABELA-32 Alleviates Doxorubicin-Induced Chronic Cardiotoxicity by Inhibiting the TGF-β/Smad Signaling Pathway.

Shuang Zhou, Zhuo Meng, Lin Lu, Junhao Xie, Lihua Li, Huilong Cheng, Kun Sun, Juxiang Wang

Abstract read
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In one paragraph

Article in Cardiovascular toxicology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

8 authors.

Shuang ZhouDepartment of Intensive Care Unit, Xiamen Cardiovascular Hospital, Xiamen University, No. 2999, Jinshan Road, Huli District, Xiamen, Fujian, China.
Zhuo MengDepartment of Pediatric Cardiology, Shanghai Children's Medical Center, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Lin LuDepartment of Intensive Care Unit, Xiamen Cardiovascular Hospital, Xiamen University, No. 2999, Jinshan Road, Huli District, Xiamen, Fujian, China.
Junhao XieDepartment of Intensive Care Unit, Xiamen Cardiovascular Hospital, Xiamen University, No. 2999, Jinshan Road, Huli District, Xiamen, Fujian, China.
Lihua LiDepartment of Intensive Care Unit, Xiamen Cardiovascular Hospital, Xiamen University, No. 2999, Jinshan Road, Huli District, Xiamen, Fujian, China.
Huilong ChengDepartment of Intensive Care Unit, Xiamen Cardiovascular Hospital, Xiamen University, No. 2999, Jinshan Road, Huli District, Xiamen, Fujian, China.
Kun SunDepartment of Pediatric Cardiology, Xinhua Hospital, School of Medicine, Shanghai Jiao Tong University, No. 1665, Kongjiang Road, Yangpu District, Shanghai, China. sunkun@xinhuamed.com.cn.
Juxiang WangDepartment of Intensive Care Unit, Xiamen Cardiovascular Hospital, Xiamen University, No. 2999, Jinshan Road, Huli District, Xiamen, Fujian, China. xmwjx2012@xmu.edu.cn.

Funding

Fujian Provincial Health Commission 2022QNB018the key project of National Natural Science Foundation 82130015
6 · The paper itself

Abstract

Cardiac fibrosis, oxidative stress, and cardiomyocyte apoptosis are key contributors to the progression of doxorubicin (DOX)-induced cardiotoxicity. ELABELA (ELA) is an early endogenous ligand of apelin receptor (APJ/APLNR), which is a G protein-coupled receptor with seven transmembrane domains. Our present study aimed to investigate the protective role and underlying mechanism of ELA-32 in mitigating oxidative stress and fibrosis associated with DOX-induced cardiotoxicity. Using a mouse model of chronic DOX cardiotoxicity (5 mg/kg, i.p, once a week for four times, the total cumulative dose is 20 mg/kg), it was found that exogenous administration of ELA-32 using a microinjection pump significantly improved cardiac function, reduced oxidative stress, and myocardial fibrosis, and enhanced survival. Furthermore, pretreatment with ELA-32 peptide protected rat cardiomyocytes (H9C2 cells) from DOX-induced cytotoxicity in vitro. However, these cardioprotective effects of ELA-32 were no longer observed after activation of the Smad signaling pathway using TGF-β1. In summary, ELA-32 attenuated DOX-induced cardiac fibrosis through by modulating the TGF-β/Smad signaling pathway, thus highlighting its potential as a therapeutic agent for preventing chronic DOX-related cardiotoxicity.

Indexed as

DoxorubicinHeart DiseasesMyocytes, CardiacSmad ProteinsTransforming Growth Factor beta1AnimalsAntibiotics, AntineoplasticCardiotoxicityCell LineDisease Models, AnimalFibrosisMaleMiceMice, Inbred C57BLOxidative StressRatsAntibiotics, AntineoplasticDoxorubicinSmad ProteinsTgfb1 protein, mouseTransforming Growth Factor beta1APJCardio-protective effectDoxorubicinELABELASmad

Identifiers

PMID40389799

What Socratic holds

Textmetadata
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.