Evidence map›Paper›PMID 38886316›Full record

ArticleJournal of cardiovascular translational research2024

Vaccarin Ameliorates Doxorubicin-Induced Cardiotoxicity via Inhibition of p38 MAPK Mediated Mitochondrial Dysfunction.

Xin Shi, Yang Cao, Hongyu Wang, Qi Zhao, Cong Yan, Shengzhu Li, Ling Jing

Abstract read
In one paragraph

Article in Journal of cardiovascular translational research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

5 citing papers in PubMed.

  1. Review
  2. Article
  3. Best Paper of the Year 2024.Journal of cardiovascular translational research · 2025
    Article
  4. Review
  5. Review
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

7 authors.

Xin Shi *Department of Cardiology, First Affiliated Hospital of Harbin Medical University, 23 Youzheng Street, Nangang Qu, Harbin, 150001, Heilongjiang, China.
Yang Cao *Department of Cardiology, First Affiliated Hospital of Harbin Medical University, 23 Youzheng Street, Nangang Qu, Harbin, 150001, Heilongjiang, China.
Hongyu WangDepartment of Cardiology, First Affiliated Hospital of Harbin Medical University, 23 Youzheng Street, Nangang Qu, Harbin, 150001, Heilongjiang, China.
Qi ZhaoDepartment of Cardiology, First Affiliated Hospital of Harbin Medical University, 23 Youzheng Street, Nangang Qu, Harbin, 150001, Heilongjiang, China.
Cong YanDepartment of Cardiology, First Affiliated Hospital of Harbin Medical University, 23 Youzheng Street, Nangang Qu, Harbin, 150001, Heilongjiang, China.
Shengzhu LiDepartment of Cardiology, First Affiliated Hospital of Harbin Medical University, 23 Youzheng Street, Nangang Qu, Harbin, 150001, Heilongjiang, China.
Ling JingDepartment of Cardiology, First Affiliated Hospital of Harbin Medical University, 23 Youzheng Street, Nangang Qu, Harbin, 150001, Heilongjiang, China. jingling0451@163.com.ORCID http://orcid.org/0009-0000-6964-7804

Funding

Heilongjiang Postdoctoral Science Foundation LBH-Z22214
6 · The paper itself

Abstract

Doxorubicin is a frequently used chemotherapeutic agent for treating various malignancies. However, it leads to severe cardiotoxic side effects, such as heart failure, and elevates the risk of sudden cardiac death among cancer patients. While oxidative stress has been identified as the primary cause of doxorubicin-induced cardiotoxicity, therapeutic antioxidant approaches have yielded unsatisfactory outcomes. The aim of this study is to explore the therapeutic potential of vaccarin, an active flavonoid glycoside extracted from traditional Chinese herbal agent Semen Vaccariae, in doxorubicin-induced cardiotoxicity. We observed that vaccarin significantly ameliorates doxorubicin-induced heart dysfunction in mouse model and suppresses oxidative stress mediated cell apoptosis via specifically inhibiting the activation of p38 MAPK pathway. In vitro, we observed that vaccarin alleviates doxorubicin-induced mitochondrial membrane depolarization and ROS generation in H9c2 cell, but the p38 MAPK agonist anisomycin reverses these effects. Our findings provide a promising natural antioxidant to protect against DOX-induced cardiotoxicity.

Indexed as

AntioxidantsApoptosisCardiotoxicityDisease Models, AnimalDoxorubicinMembrane Potential, MitochondrialMice, Inbred C57BLMitochondria, HeartMyocytes, CardiacOxidative Stressp38 Mitogen-Activated Protein KinasesReactive Oxygen SpeciesSignal TransductionAnimalsCell LineGlycosidesAntioxidantsDoxorubicinGlycosidesp38 Mitogen-Activated Protein KinasesProtein Kinase InhibitorsReactive Oxygen SpeciesAntioxidantCardiotoxicityDoxorubicinMitochondrial dysfunctionp38 MAPKVaccarin

Identifiers

PMID38886316
PMCPMC11519163

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Registered trials

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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.