Evidence map›Paper›PMID 35344140›Full record

ArticleCardiovascular toxicology2022

Exosomes Derived from Mesenchymal Stem Cells Ameliorate the Progression of Atherosclerosis in ApoE

Nan Zhang, Yuxin Luo, Huaping Zhang, Feng Zhang, Xiang Gao, Jiawei Shao

Abstract read
PubMed Publisher
In one paragraph

Article in Cardiovascular toxicology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.3field-weighted citation impact, top 10% 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

17 citing papers in PubMed, 27 citations in OpenAlex.

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  10. Development of stem cell therapy for atherosclerosis.Molecular and cellular biochemistry · 2024
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  11. The Role of Stem Cells in the Treatment of Cardiovascular Diseases.International journal of molecular sciences · 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.

Nan ZhangDepartment of Vascular Surgery, the Second Hospital of Hebei Medical University, No. 215, Heping West Road, Shijiazhuang, 050000, Hebei, People's Republic of China. zhangnan_681@163.com.
Yuxin LuoDeparment of Gastroenterology, the Second Hospital of Hebei Medical University, Shijiazhuang, 050000, Hebei, People's Republic of China.
Huaping ZhangDeparment of Critical Care Medicine, Shijiazhuang People's Hospital, Shijiazhuang, 050030, Hebei, People's Republic of China.
Feng ZhangDepartment of Vascular Surgery, the Second Hospital of Hebei Medical University, No. 215, Heping West Road, Shijiazhuang, 050000, Hebei, People's Republic of China.
Xiang GaoDepartment of Vascular Surgery, the Second Hospital of Hebei Medical University, No. 215, Heping West Road, Shijiazhuang, 050000, Hebei, People's Republic of China.
Jiawei ShaoDepartment of Vascular Surgery, the Second Hospital of Hebei Medical University, No. 215, Heping West Road, Shijiazhuang, 050000, Hebei, People's Republic of China.
Hebei Medical University · CNFirst Hospital of Shijiazhuang · CNSecond Hospital of Hebei Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Exosomes (EXO) are extracellular vesicles with lipid bilayer membrane structure containing noncoding RNA, DNA, and other molecules which mediate biological functions. The importance of EXO derived from mesenchymal stem cells (MSCs) has been underlined in cardiovascular diseases. However, the functional role of long non-coding RNA (lncRNA) released by MSCs-EXO on atherosclerosis (AS) was unknown. We aimed to investigate the effects of lncRNA fetal-lethal non-coding developmental regulatory RNA (FENDRR) released from MSC-derived EXO on AS. The accumulation of oxidized low-density lipoprotein (oxLDL) caused AS in mice and damage to human vascular endothelial cells (HUV-EC-C). MSC-EXO restored HUV-EC-C activity and alleviated arterial injury. LncRNA microarrays revealed that FENDRR was delivered to cells and tissues by MSC-EXO. FENDRR bound to microRNA (miR)-28 to regulate TEA domain transcription factor 1 (TEAD1) expression. Moreover, FENDRR knockdown exacerbated cell injury and arterial injury in mice. miR-28 inhibitor reversed the effects of FENDRR silencing and reduced atherosclerotic plaque formation. While loss of TEAD1 mitigated the effect of miR-28 inhibitor and accentuated HUV-EC-C injury in vitro and AS symptoms in vivo. Our results demonstrated that MSC-EXO secreted FENDRR to treat AS. FENDRR competed with TEAD1 to bind to miR-28, thereby reducing HUV-EC-C injury and atherosclerotic plaque formation.

Indexed as

AtherosclerosisExosomesMesenchymal Stem CellsMicroRNAsPlaque, AtheroscleroticRNA, Long NoncodingAnimalsEndothelial CellsMiceMice, Knockout, ApoEMicroRNAsRNA, Long NoncodingAtherosclerosisLong non-coding RNA FENDRRMesenchymal stem cellsmicroRNA-28; TEAD1

Identifiers

PMID35344140
OpenAlexW4220846815

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.