Evidence map›Paper›PMID 32589721›Full record

ArticleCardiovascular research2021

Single-cell RNA sequencing reveals cell type- and artery type-specific vascular remodelling in male spontaneously hypertensive rats.

Jun Cheng, Wenduo Gu, Ting Lan, Jiacheng Deng, Zhichao Ni, Zhongyi Zhang, Yanhua Hu, Xiaolei Sun, Yan Yang, Qingbo Xu

Open access · greenAbstract readComparative Study
In one paragraph

Article in Cardiovascular research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 1 pooled it
2.3field-weighted citation impact, top 11% 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

25 citing papers in PubMed, 1 synthesis or guideline pooled it, 52 citations in OpenAlex.

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  14. Single cell 'omic profiles of human aortic endothelial cellsbioRxiv : the preprint server for biology · 2024
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  18. The Aging Aorta: Are We Only as Old as Our Endothelium?Arteriosclerosis, thrombosis, and vascular biology · 2022
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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

10 authors at 2 institutions in 2 countries.

Jun ChengKey Laboratory of Medical Electrophysiology of Ministry of Education and Medical Electrophysiological Key Laboratory of Sichuan Province, Collaborative Innovation Center for Prevention and Treatment of Cardiovascular Disease, Institute of Cardiovascular Research, Southwest Medical University, 319 Zhongshan Road, Luzhou 646000, China.
Wenduo GuSchool of Cardiovascular Medicine and Sciences, King's College London BHF Centre, 125 Coldharbour Lane, London SE5 9NU, UK.
Ting LanKey Laboratory of Medical Electrophysiology of Ministry of Education and Medical Electrophysiological Key Laboratory of Sichuan Province, Collaborative Innovation Center for Prevention and Treatment of Cardiovascular Disease, Institute of Cardiovascular Research, Southwest Medical University, 319 Zhongshan Road, Luzhou 646000, China.
Jiacheng DengSchool of Cardiovascular Medicine and Sciences, King's College London BHF Centre, 125 Coldharbour Lane, London SE5 9NU, UK.
Zhichao NiSchool of Cardiovascular Medicine and Sciences, King's College London BHF Centre, 125 Coldharbour Lane, London SE5 9NU, UK.
Zhongyi ZhangSchool of Cardiovascular Medicine and Sciences, King's College London BHF Centre, 125 Coldharbour Lane, London SE5 9NU, UK.
Yanhua HuSchool of Cardiovascular Medicine and Sciences, King's College London BHF Centre, 125 Coldharbour Lane, London SE5 9NU, UK.
Xiaolei SunKey Laboratory of Medical Electrophysiology of Ministry of Education and Medical Electrophysiological Key Laboratory of Sichuan Province, Collaborative Innovation Center for Prevention and Treatment of Cardiovascular Disease, Institute of Cardiovascular Research, Southwest Medical University, 319 Zhongshan Road, Luzhou 646000, China.
Yan YangKey Laboratory of Medical Electrophysiology of Ministry of Education and Medical Electrophysiological Key Laboratory of Sichuan Province, Collaborative Innovation Center for Prevention and Treatment of Cardiovascular Disease, Institute of Cardiovascular Research, Southwest Medical University, 319 Zhongshan Road, Luzhou 646000, China.
Qingbo XuKey Laboratory of Medical Electrophysiology of Ministry of Education and Medical Electrophysiological Key Laboratory of Sichuan Province, Collaborative Innovation Center for Prevention and Treatment of Cardiovascular Disease, Institute of Cardiovascular Research, Southwest Medical University, 319 Zhongshan Road, Luzhou 646000, China.
King's College London · GBSouthwest Medical University · CN

Funding

British Heart Foundation RG/14/6/31144
6 · The paper itself

Abstract

aimsHypertension is a major risk factor for cardiovascular diseases. However, vascular remodelling, a hallmark of hypertension, has not been systematically characterized yet. We described systematic vascular remodelling, especially the artery type- and cell type-specific changes, in hypertension using spontaneously hypertensive rats (SHRs). METHODS AND

resultsSingle-cell RNA sequencing was used to depict the cell atlas of mesenteric artery (MA) and aortic artery (AA) from SHRs. More than 20 000 cells were included in the analysis. The number of immune cells more than doubled in aortic aorta in SHRs compared to Wistar Kyoto controls, whereas an expansion of MA mesenchymal stromal cells (MSCs) was observed in SHRs. Comparison of corresponding artery types and cell types identified in integrated datasets unravels dysregulated genes specific for artery types and cell types. Intersection of dysregulated genes with curated gene sets including cytokines, growth factors, extracellular matrix (ECM), receptors, etc. revealed vascular remodelling events involving cell-cell interaction and ECM re-organization. Particularly, AA remodelling encompasses upregulated cytokine genes in smooth muscle cells, endothelial cells, and especially MSCs, whereas in MA, change of genes involving the contractile machinery and downregulation of ECM-related genes were more prominent. Macrophages and T cells within the aorta demonstrated significant dysregulation of cellular interaction with vascular cells.

conclusionOur findings provide the first cell landscape of resistant and conductive arteries in hypertensive animal models. Moreover, it also offers a systematic characterization of the dysregulated gene profiles with unbiased, artery type-specific and cell type-specific manners during hypertensive vascular remodelling.

Indexed as

RNA-SeqSingle-Cell AnalysisTranscriptomeAnimalsAortaDisease Models, AnimalGene Regulatory NetworksHypertensionMaleMesenteric ArteriesRatsRats, Inbred SHRRats, Inbred WKYVascular RemodelingCell atlasCellular communicationHypertensionSingle-cell RNA sequencing

Identifiers

PMID32589721
PMCPMC7983007
OpenAlexW3038066107

What OpenQuestion holds

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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.