Evidence map›Paper›PMID 32355801›Full record

ArticleAnnals of translational medicine2020

Telomere dysfunction promotes small vessel vasculitis via the LL37-NETs-dependent mechanism.

Yingying Lu, Hong Jiang, Bingjue Li, Luxi Cao, Qixia Shen, Weiwei Yi, Zhenyu Ju, Liangliang Chen, Fei Han, Daniel Appelgren and 4 more

Open access · diamondAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Annals of translational medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.5field-weighted citation impact, top 39% 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

3 citing papers in PubMed, 11 citations in OpenAlex.

  1. Review
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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

14 authors at 5 institutions in 3 countries.

Yingying LuKidney Disease Center, The First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou 310003, China.
Hong JiangKidney Disease Center, The First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou 310003, China.
Bingjue LiKidney Disease Center, The First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou 310003, China.
Luxi CaoKidney Disease Center, The First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou 310003, China.
Qixia ShenKidney Disease Center, The First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou 310003, China.
Weiwei YiInstitute of Aging Research and Max-Planck-Research Group on Stem Cell Aging, Hangzhou Normal University, Hangzhou 311121, China.
Zhenyu JuInstitute of Aging Research and Max-Planck-Research Group on Stem Cell Aging, Hangzhou Normal University, Hangzhou 311121, China.
Liangliang ChenKidney Disease Center, The First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou 310003, China.
Fei HanKidney Disease Center, The First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou 310003, China.
Daniel AppelgrenDepartment of Medical and Health Sciences (IMH), Linkoping University, Linkoping, Sweden.
Mårten SegelmarkDepartment of Medical and Health Sciences (IMH), Linkoping University, Linkoping, Sweden.
Nicole de BuhrDepartment of Physiological Chemistry, University of Veterinary Medicine Hannover, Hannover, Germany.
Maren von Köckritz-BlickwedeDepartment of Physiological Chemistry, University of Veterinary Medicine Hannover, Hannover, Germany.
Jianghua ChenKidney Disease Center, The First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou 310003, China.
State Administration of Traditional Chinese Medicine of the People's Republic of China · CNZhejiang University · CNHangzhou Normal University · CNLinköping University · SEUniversity of Veterinary Medicine Hannover, Foundation · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSmall vessel vasculitis (SVV) is a group of systemic autoimmune diseases that are mediated by neutrophil extracellular traps (NETs) in response to cathelicidin LL37, an aging molecular marker, which could be induced by telomere dysfunction. Therefore, in this study, we evaluated the hypothesis that telomere dysfunction in neutrophils may promote SVV via an LL37-NETs-dependent mechanism.

methodsWe contrasted the release of neutrophil NETs from mice with telomere dysfunction, mice with DNA damage and wide-type mice. Neutrophil telomere length, the expression of LL37, and the formation of NETs were measured in SVV patients and healthy controls (HCs). The co-expression of γH2AX, LL37, and NETs were detected in SVV patients to evaluate the association of the immune aging of neutrophils and pro-inflammatory conditions. LL37 inhibitor was used to verify its key role in NETs release in SVV patients and DNA damage mice.

resultsWe found that NETs were over-induced by telomere dysfunction and DNA damage in mice, which may be associated with a marked increase in LL37. For patients with SVV, telomeres in neutrophils were significantly shortened, which was also associated with higher levels of LL37 and NETs. Inhibition of LL37 reduced the NETs released from neutrophils.

conclusionsTaken together, the results of these studies suggest that dysfunction of telomeres may promote SVV through the mechanism of LL37-dependent NETs. Thus, targeting the LL37-NETs may be a novel therapy for SVV.

Indexed as

DNA damageLL37neutrophil extracellular traps (NETs)small vessel vasculitis (SVV)Telomere dysfunction

Identifiers

PMID32355801
PMCPMC7186648
OpenAlexW3014282840

What OpenQuestion holds

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Registered trials

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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.