Evidence map›Paper›PMID 35842695›Full record

ArticleJournal of nanobiotechnology2022

Protective role of small extracellular vesicles derived from HUVECs treated with AGEs in diabetic vascular calcification.

Bei Guo, Su-Kang Shan, Feng Xu, Xiao Lin, Fu-Xing-Zi Li, Yi Wang, Qiu-Shuang Xu, Ming-Hui Zheng, Li-Min Lei, Chang-Chun Li and 5 more

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 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
3.6field-weighted citation impact, top 6% 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

24 citing papers in PubMed, 41 citations in OpenAlex.

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  9. Research progress on small extracellular vesicles in diabetic nephropathy.Frontiers in cell and developmental biology · 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

15 authors at 1 institution in 1 country.

Bei GuoNational Clinical Research Center for Metabolic Diseases, Department of Metabolism and Endocrinology, The Second Xiangya Hospital, Central South University, Changsha, 410000, China.
Su-Kang ShanNational Clinical Research Center for Metabolic Diseases, Department of Metabolism and Endocrinology, The Second Xiangya Hospital, Central South University, Changsha, 410000, China.
Feng XuNational Clinical Research Center for Metabolic Diseases, Department of Metabolism and Endocrinology, The Second Xiangya Hospital, Central South University, Changsha, 410000, China.
Xiao LinDepartment of Radiology, The Second Xiangya Hospital, Central South University, Changsha, Hunan, People's Republic of China.
Fu-Xing-Zi LiNational Clinical Research Center for Metabolic Diseases, Department of Metabolism and Endocrinology, The Second Xiangya Hospital, Central South University, Changsha, 410000, China.
Yi WangNational Clinical Research Center for Metabolic Diseases, Department of Metabolism and Endocrinology, The Second Xiangya Hospital, Central South University, Changsha, 410000, China.
Qiu-Shuang XuNational Clinical Research Center for Metabolic Diseases, Department of Metabolism and Endocrinology, The Second Xiangya Hospital, Central South University, Changsha, 410000, China.
Ming-Hui ZhengNational Clinical Research Center for Metabolic Diseases, Department of Metabolism and Endocrinology, The Second Xiangya Hospital, Central South University, Changsha, 410000, China.
Li-Min LeiNational Clinical Research Center for Metabolic Diseases, Department of Metabolism and Endocrinology, The Second Xiangya Hospital, Central South University, Changsha, 410000, China.
Chang-Chun LiNational Clinical Research Center for Metabolic Diseases, Department of Metabolism and Endocrinology, The Second Xiangya Hospital, Central South University, Changsha, 410000, China.
Zhi-Ang ZhouDepartment of Cardiovascular Surgery, The Second Xiangya Hospital, Central South University, Changsha, Hunan, People's Republic of China.
Muhammad Hasnain Ehsan UllahNational Clinical Research Center for Metabolic Diseases, Department of Metabolism and Endocrinology, The Second Xiangya Hospital, Central South University, Changsha, 410000, China.
Feng WuDepartment of Pathology, The Second Xiangya Hospital, Central South University, Changsha, Hunan, People's Republic of China.
Xiao-Bo LiaoDepartment of Cardiovascular Surgery, The Second Xiangya Hospital, Central South University, Changsha, Hunan, People's Republic of China.
Ling-Qing YuanNational Clinical Research Center for Metabolic Diseases, Department of Metabolism and Endocrinology, The Second Xiangya Hospital, Central South University, Changsha, 410000, China. allenylq@csu.edu.cn.ORCID http://orcid.org/0000-0001-8602-7113
Central South University · CN

Funding

Fundamental Research Funds for Central Universities of the Central South University 2021zzts0387Key R&D Plan of Hunan Province 2020SK2078National Natural Science Foundation of China 81770881National Natural Science Foundation of China 81870623National Natural Science Foundation of China 82070910Natural Science Foundation of Hunan Province 2021JJ30036
6 · The paper itself

Abstract

The pathogenesis of vascular calcification in diabetic patients remains elusive. As an effective information transmitter, small extracellular vesicles (sEVs) carry abundant microRNAs (miRNAs) that regulate the physiological and pathological states of recipient cells. In the present study, significant up-regulation of miR-126-5p was observed in sEVs isolated from human umbilical vein endothelial cells (HUVECs) stimulated with advanced glycation end-products (A-EC/sEVs). Intriguingly, these sEVs suppressed the osteogenic differentiation of vascular smooth muscle cells (VSMCs) by targeting BMPR1B, which encodes the receptor for BMP, thereby blocking the smad1/5/9 signalling pathway. In addition, knocking down miR-126-5p in HUVECs significantly diminished the anti-calcification effect of A-EC/sEVs in a mouse model of type 2 diabetes. Overall, miR-126-5p is highly enriched in sEVs derived from AGEs stimulated HUVECs and can target BMPR1B to negatively regulate the trans-differentiation of VSMCs both in vitro and in vivo.

Indexed as

Diabetes Mellitus, Type 2Extracellular VesiclesMicroRNAsVascular CalcificationAnimalsHumansHuman Umbilical Vein Endothelial CellsMiceOsteogenesisMicroRNAsDiabetesEndothelial cellsmiR-126-5psEVsVascular calcification

Identifiers

PMID35842695
PMCPMC9287893
OpenAlexW4285588471

What OpenQuestion holds

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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.