Evidence map›Paper›PMID 37256416›Full record

ArticleCardiovascular drugs and therapy2024

CTRP5 Attenuates Doxorubicin-Induced Cardiotoxicity Via Inhibiting TLR4/NLRP3 Signaling.

Zhaoxia Zhang, Jianye Peng, Yewen Hu, Gaofeng Zeng, Weiping Du, Caijie Shen

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Article in Cardiovascular drugs and therapy, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
2.0field-weighted citation impact, top 12% 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

7 citing papers in PubMed, 9 citations in OpenAlex.

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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

6 authors at 2 institutions in 1 country.

Zhaoxia Zhang *Department of Cardiology, The First Affiliated Hospital of Ningbo University, #59 Liuting Street, Haishu District, Ningbo, Zhejiang, China.
Jianye Peng *Department of Cardiology, The Second Affiliated Hospital of Hengyang, Hengyang Medcial School, University of South China, Hengyang, 421001, Hunan, China.
Yewen HuDepartment of Cardiology, The First Affiliated Hospital of Ningbo University, #59 Liuting Street, Haishu District, Ningbo, Zhejiang, China.
Gaofeng ZengDepartment of Cardiology, The First Affiliated Hospital of Ningbo University, #59 Liuting Street, Haishu District, Ningbo, Zhejiang, China.
Weiping DuDepartment of Cardiology, The First Affiliated Hospital of Ningbo University, #59 Liuting Street, Haishu District, Ningbo, Zhejiang, China. duweiping@163.com.
Caijie ShenDepartment of Cardiology, The First Affiliated Hospital of Ningbo University, #59 Liuting Street, Haishu District, Ningbo, Zhejiang, China. shenzihai1101@126.com.ORCID 0000-0002-6971-0313
Ningbo University · CNUniversity of South China · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundC1q/tumor necrosis factor-related protein 5 (CTRP5) has been reported to be a crucial regulator in cardiac ischemia/reperfusion (I/R) injury. Nevertheless, the potential role of CTRP5 in doxorubicin (DOX)-induced cardiotoxicity and the potential mechanisms remain largely unclear.

methodsWe overexpressed CTRP5 in the hearts using an adeno-associated virus 9 (AAV9) system through tail vein injection. C57BL/6 mice were subjected to DOX (15 mg/kg/day, i.p.) to generate DOX-induced cardiotoxicity for 4 weeks. Subsequently, cardiac staining and molecular biological analysis were performed to analyze the morphological and biochemical effects of CTRP5 on the cardiac injury. H9c2 cells were used for validation in vitro.

resultsCTRP5 expression was down-regulated after DOX treatment both in vivo and in vitro. CTRP5 overexpression significantly attenuated DOX-induced cardiac injury, cardiac dysfunction, inhibited oxidative stress and inflammatory response. Mechanistically, CTRP5 overexpression markedly decreased the protein expression of toll-like receptor 4 (TLR4), NLRP3, cleaved caspase-1 and caspase-1, indicating TLR/NLRP3 signaling contributes to the cardioprotective role of CTRP5 in DOX-induced cardiotoxicity.

conclusionsTogether, our findings demonstrated that CTRP5 overexpression could protect the heart from oxidative stress and inflammatory injury induced by DOX through inhibiting TLR4/NLRP3 signaling, suggesting that CTRP5 might be a potential therapeutic target in the prevention of DOX-induced cardiotoxicity.

Indexed as

CardiotoxicityDoxorubicinMice, Inbred C57BLMyocytes, CardiacNLR Family, Pyrin Domain-Containing 3 ProteinOxidative StressSignal TransductionToll-Like Receptor 4AdipokinesAnimalsCell LineDisease Models, AnimalHeart DiseasesMaleMiceRatsAdipokinesCORS26 protein, mouseDoxorubicinNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, mouseTlr4 protein, mouseToll-Like Receptor 4cardiotoxicityCTRP5DoxorubicininflammationNLRP3 inflammasomeoxidative stress

Identifiers

PMID37256416
OpenAlexW4378781523

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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.