Evidence map›Paper›PMID 36077544›Full record

ArticleInternational journal of molecular sciences2022

Dapagliflozin Mitigates Doxorubicin-Caused Myocardium Damage by Regulating AKT-Mediated Oxidative Stress, Cardiac Remodeling, and Inflammation.

Pei-Ling Hsieh, Pei-Ming Chu, Hui-Ching Cheng, Yu-Ting Huang, Wan-Ching Chou, Kun-Ling Tsai, Shih-Hung Chan

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed
16.4field-weighted citation impact, top 1% of its field
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

65 citing papers in PubMed, 108 citations in OpenAlex.

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  16. Drug Repositioning in Doxorubicin-Induced Cardiotoxicity Protection.International journal of molecular sciences · 2025
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5 more citing papers are in PubMed but not listed here.

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 at 4 institutions in 1 country.

Pei-Ling HsiehDepartment of Anatomy, School of Medicine, China Medical University, Taichung 404, Taiwan.
Pei-Ming ChuDepartment of Anatomy, School of Medicine, Chung Shan Medical University, Taichung 402, Taiwan.
Hui-Ching ChengDepartment of Physical Therapy, College of Medicine, National Cheng Kung University, Tainan 701, Taiwan.
Yu-Ting HuangDepartment of Physical Therapy, College of Medicine, National Cheng Kung University, Tainan 701, Taiwan.
Wan-Ching ChouDepartment of Physical Therapy, College of Medicine, National Cheng Kung University, Tainan 701, Taiwan.
Kun-Ling TsaiDepartment of Physical Therapy, College of Medicine, National Cheng Kung University, Tainan 701, Taiwan.ORCID 0000-0002-3814-1453
Shih-Hung ChanDepartment of Internal Medicine, College of Medicine, National Cheng Kung University Hospital, National Cheng Kung University, Tainan 704, Taiwan.
National Cheng Kung University · TWChina Medical University · TWChung Shan Medical University · TWNational Cheng Kung University Hospital · TW

Funding

National Cheng Kung University Hospital NCKUH-11002005
6 · The paper itself

Abstract

Doxorubicin (Dox) is a commonly used anthracycline chemotherapy with a side effect of cardiotoxicity, which may increase the risk of heart failure for cancer patients. Although various studies have demonstrated the cardioprotective property of dapagliflozin (DAPA), a sodium-glucose cotransporter 2 inhibitor, the detailed mechanism underlying its effect on Dox-induced cardiomyopathy is still limited. In this study, we showed that DAPA induced the activation of AKT/PI3K signaling in cardiac myoblast H9c2 cells following Dox treatment, leading to the upregulation of antioxidant HO-1, NQO1, and SOD, as well as an improved mitochondrial dysfunction via Nrf2. In addition, the reduced oxidative stress resulted in the downregulation of hypertrophy (ANP and BNP) and fibrosis (phospho-Smad3, collagen I, fibronectin, and α-SMA) markers. Furthermore, the inflammatory IL-8 concentration was inhibited after DAPA, possibly through PI3K/AKT/Nrf2/p38/NF-κB signaling. Moreover, our results were validated in vivo, and echocardiography results suggested an improved cardiac function in DAPA-receiving rats. In summary, we demonstrated that the administration of DAPA could mitigate the Dox-elicited cardiotoxicity by reducing oxidative stress, mitochondrial dysfunction, fibrosis, hypertrophy, and inflammation via PI3K/AKT/Nrf2 signaling.

Indexed as

CardiotoxicityNF-E2-Related Factor 2AnimalsApoptosisBenzhydryl CompoundsDoxorubicinFibrosisGlucosidesHypertrophyInflammationMyocardiumMyocytes, CardiacOxidative StressPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktRatsBenzhydryl CompoundsdapagliflozinDoxorubicinGlucosidesNF-E2-Related Factor 2Phosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktAktcardiotoxicitydapagliflozindoxorubicin

Identifiers

PMID36077544
PMCPMC9456438
OpenAlexW4294733487

What OpenQuestion holds

Textmetadata
LicenceCC BY
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 OpenQuestion graph.