Evidence map›Paper›PMID 37540334›Full record

ArticleDrug delivery and translational research2024

hUC-MSC-EV-miR-24 enhances the protective effect of dexmedetomidine preconditioning against myocardial ischemia-reperfusion injury through the KEAP1/Nrf2/HO-1 signaling.

Zixin Hou, Fengrui Yang, Kemin Chen, Yuxia Wang, Jie Qin, Feng Liang

Abstract read
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In one paragraph

Article in Drug delivery and translational research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
6.5field-weighted citation impact, top 3% 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

21 citing papers in PubMed, 42 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 3 institutions in 1 country.

Zixin HouDepartment of Anesthesiology, Hengyang Medical School, The First Affiliated Hospital, University of South China, Hengyang, 421001, People's Republic of China.
Fengrui YangDepartment of Anesthesiology, Hengyang Medical School, The First Affiliated Hospital, University of South China, Hengyang, 421001, People's Republic of China.
Kemin ChenDepartment of Anesthesiology, Hengyang Medical School, The First Affiliated Hospital, University of South China, Hengyang, 421001, People's Republic of China.
Yuxia WangDepartment of Anesthesiology, Hengyang Medical School, The First Affiliated Hospital, University of South China, Hengyang, 421001, People's Republic of China.
Jie QinDepartment of Anesthesiology, Hengyang Medical School, The First Affiliated Hospital, University of South China, Hengyang, 421001, People's Republic of China.
Feng LiangDepartment of Anesthesiology, Hengyang Medical School, The First Affiliated Hospital, University of South China, Hengyang, 421001, People's Republic of China. 275449729@qq.com.
University of South China · CNFirst Affiliated Hospital of University of South China · CNHuaihua University · CN

Funding

Excellent Youth Foundation of Hunan Provincial Department of Education 19B477Guiding project of Hengyang science and Technology Bureau 202121034637Natural Science Foundation of Hunan Province 2021JJ70043Project of Hunan Provincial Health Commission 20200018Project of Hunan Provincial Health Commission 20200037
6 · The paper itself

Abstract

The cardioprotective effect of microRNAs (miRNAs) on myocardial ischemic-reperfusion (I/R) injury has been documented. Here, we aim to decipher the mechanism of miR-24 delivered by human umbilical cord mesenchymal stem cell-derived extracellular vesicles (hUC-MSC-EVs) in myocardial I/R injury after dexmedetomidine (DEX) preconditioning. We collected and identified hUC-MSCs and extracted EVs, which were co-cultured with DEX-preconditioned hypoxia/reoxygenation (H/R) cardiomyocyte models or injected into I/R mouse models. The cardiomyocytes and myocardial injury were evaluated by molecular biology experiments. miR-24 was highly expressed in hUC-MSC-EVs. hUC-MSC-EVs could transfer miR-24 into cardiomyocytes where miR-24 augmented cell viability and inhibited cell apoptosis after DEX preconditioning. In the co-culture system of RAW264.7 macrophages with hUC-MSC-EVs, miR-24 promoted M2-type polarization of macrophages and reduced M1-type macrophage polarization. Mechanistically, miR-24 targeted KEAP1 and inhibited its expression, resulting in disruption of the Nrf2/HO-1 signaling. In vivo data confirmed that miR-24 delivered by hUC-MSC-EVs enhanced the suppressing effect of DEX preconditioning on inflammation and apoptosis in rats following myocardial I/R injury. Overall, miR-24 delivered by hUC-MSC-EVs can promote M2 polarization of macrophages and enhance the protective effect of DEX preconditioning on myocardial I/R injury by down-regulating the KEAP1/Nrf2/HO-1 signaling axis.

Indexed as

DexmedetomidineMicroRNAsMyocardial Reperfusion InjuryAnimalsHumansKelch-Like ECH-Associated Protein 1MiceNF-E2-Related Factor 2RatsDexmedetomidineKEAP1 protein, humanKEAP1 protein, ratKelch-Like ECH-Associated Protein 1MicroRNAsMIRN24 microRNA, humanMIRN24 microRNA, ratNF-E2-Related Factor 2DexmedetomidineExtracellular vesiclesHuman umbilical cord mesenchymal stem cellsIschemic-reperfusion injuryKEAP1Macrophage polarizationmicroRNA-24Nrf2/HO-1 signaling pathway

Identifiers

PMID37540334
OpenAlexW4385563548

What OpenQuestion 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 OpenQuestion graph.