Evidence map›Paper›PMID 35139878›Full record

ArticleJournal of nanobiotechnology2022

The effects of extracellular vesicles derived from Krüppel-Like Factor 2 overexpressing endothelial cells on the regulation of cardiac inflammation in the dilated cardiomyopathy.

Wenfeng Zhang, Ziwei Chen, Shuaihua Qiao, Siyuan Chen, Hongyan Zheng, Xuan Wei, Qiaoling Li, Biao Xu, Wei Huang

Open access · goldAbstract read
In one paragraph

Article in Journal of nanobiotechnology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.2field-weighted citation impact, top 23% 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

12 citing papers in PubMed, 16 citations in OpenAlex.

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  4. Small Extracellular Vesicles from Breast Cancer Cells Induce Cardiotoxicity.International journal of molecular sciences · 2025
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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

9 authors at 1 institution in 1 country.

Wenfeng Zhang *Department of Cardiology, Nanjing Drum Tower Hospital Clinical College of Nanjing Medical University, Nanjing, 210008, China.
Ziwei Chen *Department of Cardiology, Affiliated Drum Tower Hospital, Medical School of Nanjing University, Nanjing, 210008, China.
Shuaihua Qiao *Department of Cardiology, Affiliated Drum Tower Hospital, Medical School of Nanjing University, Nanjing, 210008, China.
Siyuan ChenDepartment of Cardiology, Nanjing Drum Tower Hospital Clinical College of Nanjing Medical University, Nanjing, 210008, China.
Hongyan ZhengDepartment of Cardiology, Affiliated Drum Tower Hospital, Medical School of Nanjing University, Nanjing, 210008, China.
Xuan WeiDepartment of Cardiology, Affiliated Drum Tower Hospital, Medical School of Nanjing University, Nanjing, 210008, China.
Qiaoling Li *Department of Cardiology, Affiliated Drum Tower Hospital, Medical School of Nanjing University, Nanjing, 210008, China. lqldoctor@126.com.
Biao Xu *Department of Cardiology, Nanjing Drum Tower Hospital Clinical College of Nanjing Medical University, Nanjing, 210008, China. xubiao62@nju.edu.cn.
Wei Huang *Department of Cardiology, Nanjing Drum Tower Hospital Clinical College of Nanjing Medical University, Nanjing, 210008, China. 1210252287@qq.com.ORCID http://orcid.org/0000-0002-2982-7752
Nanjing Drum Tower Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDilated cardiomyopathy (DCM) is one of the common causes of heart failure. Myocardial injury triggers an inflammatory response and recruits immune cells into the heart. High expression of Krüppel-like factor 2 (KLF2) in endothelial cells (ECs) potentially exerts an anti-inflammatory effect. However, the role of extracellular vesicles (EVs) from KLF2-overexpressing ECs (KLF2-EVs) in DCM remains unclear. METHODS AND

resultsEVs were separated from the supernatant of KLF2-overexpressing ECs by gradient centrifugation. Mice were repeatedly administered low-dose doxorubicin (DOX) and then received KLF2-EVs through an intravenous injection. Treatment with KLF2-EVs prevented doxorubicin-induced left ventricular dysfunction and reduced the recruitment of Ly6

conclusionsEVs derived from KLF2-overexpressing ECs reduced cardiac inflammation and ameliorated left ventricular dysfunction in DCM mice by targeting the CCR2 protein to inhibit Ly6C

Indexed as

Cardiomyopathy, DilatedExtracellular VesiclesAnimalsEndothelial CellsInflammationKruppel-Like Transcription FactorsMiceKruppel-Like Transcription Factors

Identifiers

PMID35139878
PMCPMC8827179
OpenAlexW4210837066

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.