Evidence map›Paper›PMID 34585365›Full record

ArticleHuman cell2022

Exosomes derived from mesenchymal stem cells ameliorate renal fibrosis via delivery of miR-186-5p.

Yiqiong Yang, Jing Wang, Yu Zhang, Xiuxiu Hu, Li Li, Pingsheng Chen

Abstract read
PubMed Publisher
In one paragraph

Article in Human cell, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.1field-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

29 citing papers in PubMed, 33 citations in OpenAlex.

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  19. Mesenchymal stem cell-derived extracellular vesicles for human diseases.Extracellular vesicles and circulating nucleic acids · 2024
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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.

Yiqiong YangDepartment of Pathology and Pathophysiology, Medical School, Southeast University, Nanjing, Jiangsu, 210009, People's Republic of China.
Jing WangInstitute of Andrology, The Affiliated Drum Tower Hospital, Nanjing University, Nanjing, Jiangsu, 210008, People's Republic of China.
Yu ZhangDepartment of Pathology and Pathophysiology, Medical School, Southeast University, Nanjing, Jiangsu, 210009, People's Republic of China.
Xiuxiu HuDepartment of Pathology and Pathophysiology, Medical School, Southeast University, Nanjing, Jiangsu, 210009, People's Republic of China.
Li LiDepartment of Pathology and Pathophysiology, Medical School, Southeast University, Nanjing, Jiangsu, 210009, People's Republic of China.
Pingsheng ChenInstitute of Nephrology, The Affiliated Zhongda Hospital, Southeast University, Dingjiaqiao 87, Gulou District, Nanjing, Jiangsu, 210009, People's Republic of China. cps18851863704@126.com.
Southeast University · CNNanjing Drum Tower Hospital · CNZhongda Hospital Southeast University · CN

Funding

key r & d program of jiangsu province, china BE2019712national natural scientific foundation of china 81370868
6 · The paper itself

Abstract

Evidence has shown that mesenchymal stem cells' (MSCs) therapy has potential application in treating chronic kidney disease (CKD). In addition, MSCs-derived exosomes can improve the renal function and prevent the progression of CKD. However, the mechanisms by which MSCs-derived exosomes (MSCs-Exo) ameliorate renal fibrosis in CKD remain largely unclear. To mimic an in vitro model of renal fibrosis, rat kidney tubular epithelial cells (NRK52E) were stimulated with transforming growth factor (TGF)-β1. In addition, we established an in vivo model of unilateral ureteric obstruction (UUO)-induced renal fibrosis. Meanwhile, we exploited exosomes derived from MSCs for delivering miR-186-5p agomir into NRK52E cells or kidneys in vitro and in vivo. In this study, we found that level of miR-186-5p was significantly downregulated in TGF-β1-stimulated NRK52E cells and the obstructed kidneys of UUO mice. In addition, miR-186-5p can be transferred from MSCs to NRK52E cells via exosomes. MSCs-delivered miR-186-5p markedly reduced the accumulation of extracellular matrix (ECM) protein, and inhibited epithelial-to-mesenchymal transition (EMT) and apoptosis in TGF-β1-stimulated NRK52E cells. Moreover, exosomal miR-186-5p from MSCs attenuated kidney injury and fibrosis in a UUO mouse model via inhibition of the ECM protein accumulation and EMT process. Meanwhile, dual-luciferase assay showed that miR-186-5p downregulated Smad5 expression via direct binding with the 3'-UTR of Smad5. Collectively then, these findings indicated that exosomal miR-186-5p derived from MSCs could attenuate renal fibrosis in vitro and in vivo by downregulation of Smad5. These findings may help to understand the role of MSCs' exosomes in alleviating renal fibrosis in CKD.

Indexed as

AnimalsApoptosisCells, CulturedDisease Models, AnimalDown-RegulationEpithelial-Mesenchymal TransitionExosomesExtracellular Matrix ProteinsFibrosisKidneyMesenchymal Stem CellsMiceMicroRNAsRatsRenal Insufficiency, ChronicSmad5 ProteinExtracellular Matrix ProteinsMicroRNAsMIRN186 microRNA, humanSmad5 ProteinSmad5 protein, mouseChronic kidney diseaseExosomesMesenchymal stem cellsRenal fibrosis

Identifiers

PMID34585365
OpenAlexW3203164466

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.