Evidence map›Paper›PMID 33203843›Full record

ArticleNature communications2020

Chromatin accessibility landscapes of skin cells in systemic sclerosis nominate dendritic cells in disease pathogenesis.

Qian Liu, Lisa C Zaba, Ansuman T Satpathy, Michelle Longmire, Wen Zhang, Kun Li, Jeffrey Granja, Chuang Guo, Jun Lin, Rui Li and 7 more

Erratum issuedOpen access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

21 citing papers in PubMed, 47 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

17 authors at 4 institutions in 3 countries.

Qian LiuDepartment of Oncology, The First Affiliated Hospital of USTC, Division of Molecular Medicine, Hefei National Laboratory for Physical Sciences at Microscale, the CAS Key Laboratory of Innate Immunity and Chronic Disease, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, 230021, China.
Lisa C ZabaCenter for Personal Dynamic Regulomes, Stanford University School of Medicine, Stanford, CA, USA.
Ansuman T SatpathyCenter for Personal Dynamic Regulomes, Stanford University School of Medicine, Stanford, CA, USA.ORCID http://orcid.org/0000-0002-5167-537X
Michelle LongmireCenter for Personal Dynamic Regulomes, Stanford University School of Medicine, Stanford, CA, USA.
Wen ZhangDepartment of Oncology, The First Affiliated Hospital of USTC, Division of Molecular Medicine, Hefei National Laboratory for Physical Sciences at Microscale, the CAS Key Laboratory of Innate Immunity and Chronic Disease, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, 230021, China.
Kun LiDepartment of Oncology, The First Affiliated Hospital of USTC, Division of Molecular Medicine, Hefei National Laboratory for Physical Sciences at Microscale, the CAS Key Laboratory of Innate Immunity and Chronic Disease, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, 230021, China.ORCID http://orcid.org/0000-0001-6550-4937
Jeffrey GranjaCenter for Personal Dynamic Regulomes, Stanford University School of Medicine, Stanford, CA, USA.
Chuang GuoDepartment of Oncology, The First Affiliated Hospital of USTC, Division of Molecular Medicine, Hefei National Laboratory for Physical Sciences at Microscale, the CAS Key Laboratory of Innate Immunity and Chronic Disease, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, 230021, China.ORCID http://orcid.org/0000-0002-3912-0793
Jun LinDepartment of Oncology, The First Affiliated Hospital of USTC, Division of Molecular Medicine, Hefei National Laboratory for Physical Sciences at Microscale, the CAS Key Laboratory of Innate Immunity and Chronic Disease, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, 230021, China.ORCID http://orcid.org/0000-0001-7087-6540
Rui LiCenter for Personal Dynamic Regulomes, Stanford University School of Medicine, Stanford, CA, USA.
Karen TolentinoCenter for Personal Dynamic Regulomes, Stanford University School of Medicine, Stanford, CA, USA.
Gabriela KaniaDepartment of Rheumatology, University Hospital Zurich, Zurich, Switzerland.
Oliver DistlerDepartment of Rheumatology, University Hospital Zurich, Zurich, Switzerland.
David FiorentinoDepartment of Dermatology, Stanford University School of Medicine, Stanford, CA, 94305, USA.
Lorinda ChungDepartment of Dermatology, Stanford University School of Medicine, Stanford, CA, 94305, USA.
Kun QuDepartment of Oncology, The First Affiliated Hospital of USTC, Division of Molecular Medicine, Hefei National Laboratory for Physical Sciences at Microscale, the CAS Key Laboratory of Innate Immunity and Chronic Disease, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, 230021, China. qukun@ustc.edu.cn.ORCID http://orcid.org/0000-0002-5555-8437
Howard Y ChangCenter for Personal Dynamic Regulomes, Stanford University School of Medicine, Stanford, CA, USA. howchang@stanford.edu.ORCID http://orcid.org/0000-0002-9459-4393
Stanford University · USUniversity of Science and Technology of China · CNStanford Medicine · USUniversity Hospital of Zurich · CH

Funding

Special EquipmentP50HG007735 · NHGRI · STANFORD UNIVERSITY · PI CHANG, HOWARD Y · 2014 to 2018
$15.2M
Howard Hughes Medical InstituteNHGRI NIH HHS P50 HG007735
6 · The paper itself

Abstract

Systemic sclerosis (SSc) is a disease at the intersection of autoimmunity and fibrosis. However, the epigenetic regulation and the contributions of diverse cell types to SSc remain unclear. Here we survey, using ATAC-seq, the active DNA regulatory elements of eight types of primary cells in normal skin from healthy controls, as well as clinically affected and unaffected skin from SSc patients. We find that accessible DNA elements in skin-resident dendritic cells (DCs) exhibit the highest enrichment of SSc-associated single-nucleotide polymorphisms (SNPs) and predict the degrees of skin fibrosis in patients. DCs also have the greatest disease-associated changes in chromatin accessibility and the strongest alteration of cell-cell interactions in SSc lesions. Lastly, data from an independent cohort of patients with SSc confirm a significant increase of DCs in lesioned skin. Thus, the DCs epigenome links inherited susceptibility and clinically apparent fibrosis in SSc skin, and can be an important driver of SSc pathogenesis.

Indexed as

Case-Control StudiesCell CommunicationChromatinEpigenomeFibrosisGenetic Predisposition to DiseaseHumansLangerhans CellsPolymorphism, Single NucleotideRegulatory Sequences, Nucleic AcidScleroderma, SystemicSkinTranscription FactorsTranscription Initiation SiteChromatinTranscription FactorsZbtb46 protein, human

Identifiers

PMID33203843
PMCPMC7672105
OpenAlexW3101260309

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.