Evidence map›Paper›PMID 36536941›Full record

ArticleInternational journal of nanomedicine2022

miR-186-5p Dysregulation in Serum Exosomes from Patients with AMI Aggravates Atherosclerosis via Targeting LOX-1.

Jiaxing Ding, Huili Li, Wei Liu, Xuehua Wang, Yu Feng, Hongquan Guan, Zhijian Chen

Open access · goldAbstract read
In one paragraph

Article in International journal of nanomedicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
2.6field-weighted citation impact, top 9% 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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 32 citations in OpenAlex.

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  18. Extracellular vesicles derived from CD4Cellular & molecular biology letters · 2023
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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

7 authors at 3 institutions in 1 country.

Jiaxing Ding *Department of Cardiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, People's Republic of China.
Huili Li *Department of Cardiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, People's Republic of China.
Wei Liu *Department of Cardiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, People's Republic of China.
Xuehua WangDepartment of Cardiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, People's Republic of China.
Yu FengDepartment of Cardiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, People's Republic of China.
Hongquan GuanDepartment of Cardiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, People's Republic of China.
Zhijian ChenDepartment of Cardiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, People's Republic of China.
Huazhong University of Science and Technology · CNUnion Hospital · CNHenan Provincial People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Purpose: The formation of macrophage-derived foam cells via the uptake of modified lipoproteins is a pivotal development event in atherosclerosis. It has been reported that clinical and experimental myocardial infarction could accelerate atherosclerosis. Several studies have suggested the critical role of exosomes in cardiovascular diseases. However, the role of exosomes from patients with acute myocardial infarction (AMI) patients in atherogenesis remains unclear. Patients and Methods: Serum exosomes from AMI patients (AMI-Exo) and control individuals (Con-Exo) were isolated and characterized. These exosomes were studied in vitro and in vivo to determine their impact on macrophage foaming and atherogenesis. Results: Our results showed that AMI-Exo promoted foam cell formation in oxidized low-density lipoprotein (ox-LDL)-treated macrophages and progression of atherosclerosis in high-fat/cholesterol diet-fed ApoE Conclusion: In conclusion, the current findings suggest that dysregulated miR-186-5p in AMI-Exo may explain the contribution of acute ischemia events to the advancement of atherosclerosis by enhancing macrophage foaming via its target, LOX-1.

Indexed as

AtherosclerosisExosomesMicroRNAsMyocardial InfarctionAnimalsHumansMiceMice, Knockout, ApoEScavenger Receptors, Class EMicroRNAsMIRN186 microRNA, humanOLR1 protein, humanScavenger Receptors, Class Eacute myocardial infarctionatherosclerosisexosomesLOX-1macrophages

Identifiers

PMID36536941
PMCPMC9758944
OpenAlexW4311178344

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.