Evidence map›Paper›PMID 35882857›Full record

ArticleCell death & disease2022

The crosstalk between endothelial cells and vascular smooth muscle cells aggravates high phosphorus-induced arterial calcification.

Xiao Lin, Su-Kang Shan, Feng Xu, Jia-Yu Zhong, Feng Wu, Jia-Yue Duan, Bei Guo, Fu-Xing-Zi Li, Yi Wang, Ming-Hui Zheng and 8 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
10.7field-weighted citation impact, top 1% 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

52 citing papers in PubMed, 76 citations in OpenAlex.

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  15. Considerations on the Development of Therapeutics in Vascular Calcification.Journal of cardiovascular development and disease · 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

18 authors at 1 institution in 1 country.

Xiao Lin *National Clinical Research Center for Metabolic Diseases, Department of Metabolism and Endocrinology, The Second Xiangya Hospital, Central South University, Changsha, 410000, China.ORCID 0000-0002-6039-3630
Su-Kang Shan *National Clinical Research Center for Metabolic Diseases, Department of Metabolism and Endocrinology, The Second Xiangya Hospital, Central South University, Changsha, 410000, China.ORCID 0000-0003-2907-2190
Feng XuNational Clinical Research Center for Metabolic Diseases, Department of Metabolism and Endocrinology, The Second Xiangya Hospital, Central South University, Changsha, 410000, China.ORCID 0000-0003-0902-2858
Jia-Yu ZhongDepartment of PET Center, the Xiangya Hospital, Central South University, Changsha, China.ORCID 0000-0002-2542-8076
Feng WuDepartment of Pathology, the Second Xiangya Hospital, Central South University, Changsha, China.
Jia-Yue DuanNational Clinical Research Center for Metabolic Diseases, Department of Metabolism and Endocrinology, The Second Xiangya Hospital, Central South University, Changsha, 410000, China.
Bei GuoNational Clinical Research Center for Metabolic Diseases, Department of Metabolism and Endocrinology, The Second Xiangya Hospital, Central South University, Changsha, 410000, China.ORCID 0000-0003-3006-7209
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.ORCID 0000-0001-9025-2604
Yi WangNational Clinical Research Center for Metabolic Diseases, Department of Metabolism and Endocrinology, The Second Xiangya Hospital, Central South University, Changsha, 410000, China.ORCID 0000-0001-8241-6971
Ming-Hui ZhengNational Clinical Research Center for Metabolic Diseases, Department of Metabolism and Endocrinology, The Second Xiangya Hospital, Central South University, Changsha, 410000, China.ORCID 0000-0002-9854-3454
Qiu-Shuang XuNational Clinical Research Center for Metabolic Diseases, Department of Metabolism and Endocrinology, The Second Xiangya Hospital, Central South University, Changsha, 410000, China.ORCID 0000-0002-7877-4159
Li-Min LeiNational Clinical Research Center for Metabolic Diseases, Department of Metabolism and Endocrinology, The Second Xiangya Hospital, Central South University, Changsha, 410000, China.ORCID 0000-0003-2934-6796
Wen-Lu Ou-YangNational Clinical Research Center for Metabolic Diseases, Department of Metabolism and Endocrinology, The Second Xiangya Hospital, Central South University, Changsha, 410000, China.ORCID 0000-0002-0610-2118
Yun-Yun WuNational Clinical Research Center for Metabolic Diseases, Department of Metabolism and Endocrinology, The Second Xiangya Hospital, Central South University, Changsha, 410000, China.ORCID 0000-0003-4639-4132
Ke-Xin TangNational Clinical Research Center for Metabolic Diseases, Department of Metabolism and Endocrinology, The Second Xiangya Hospital, Central South University, Changsha, 410000, China.ORCID 0000-0002-5735-8658
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.ORCID 0000-0002-4214-6927
Xiao-Bo LiaoDepartment of Cardiovascular Surgery, the Second Xiangya Hospital, Central South University, Changsha, 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 0000-0001-8602-7113
Central South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Arterial calcification is highly prevalent, particularly in patients with end-stage renal disease (ESRD). The osteogenic differentiation of vascular smooth muscle cells (VSMCs) is the critical process for the development of arterial calcification. However, the detailed mechanism of VSMCs calcification remains to be elucidated. Here, we investigated the role of exosomes (Exos) derived from endothelial cells (ECs) in arterial calcification and its potential mechanisms in ESRD. Accelerated VSMCs calcification was observed when VSMCs were exposed to ECs culture media stimulated by uremic serum or high concentration of inorganic phosphate (3.5 mM Pi). and the pro-calcification effect of the ECs culture media was attenuated by exosome depletion. Exosomes derived from high concentrations of inorganic phosphate-induced ECs (ECs

Indexed as

ExosomesKidney Failure, ChronicMicroRNAsVascular CalcificationAnimalsCulture MediaEndothelial CellsInsulin-Like Growth Factor IMiceMuscle, Smooth, VascularMyocytes, Smooth MuscleOsteogenesisPhosphatesPhosphorusCulture MediaInsulin-Like Growth Factor IMicroRNAsPhosphatesPhosphorus

Identifiers

PMID35882857
PMCPMC9325771
OpenAlexW4288046151

What OpenQuestion holds

Textmetadata
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.