Evidence map›Paper›PMID 32512831›Full record

ReviewInternational journal of molecular sciences2020

The Emerging Role of Innate Immunity in Chronic Kidney Diseases.

Philip Chiu-Tsun Tang, Ying-Ying Zhang, Max Kam-Kwan Chan, Winson Wing-Yin Lam, Jeff Yat-Fai Chung, Wei Kang, Ka-Fai To, Hui-Yao Lan, Patrick Ming-Kuen Tang

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
2.4field-weighted citation impact, top 10% 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

36 citing papers in PubMed, 44 citations in OpenAlex.

  1. Review
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  15. Leukocyte-endothelial interaction in CKD.Clinical kidney journal · 2023
    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

9 authors at 2 institutions in 2 countries.

Philip Chiu-Tsun TangDepartment of Anatomical and Cellular Pathology, State Key Laboratory of Translational Oncology, Prince of Wales Hospital, The Chinese University of Hong Kong, Hong Kong 999077, China.ORCID 0000-0002-1768-1127
Ying-Ying ZhangDepartment of Nephrology, Tongji Hospital, Tongji University School of Medicine, Shanghai 200065, China.
Max Kam-Kwan ChanDepartment of Anatomical and Cellular Pathology, State Key Laboratory of Translational Oncology, Prince of Wales Hospital, The Chinese University of Hong Kong, Hong Kong 999077, China.
Winson Wing-Yin LamDepartment of Anatomical and Cellular Pathology, State Key Laboratory of Translational Oncology, Prince of Wales Hospital, The Chinese University of Hong Kong, Hong Kong 999077, China.
Jeff Yat-Fai ChungDepartment of Anatomical and Cellular Pathology, State Key Laboratory of Translational Oncology, Prince of Wales Hospital, The Chinese University of Hong Kong, Hong Kong 999077, China.
Wei KangDepartment of Anatomical and Cellular Pathology, State Key Laboratory of Translational Oncology, Prince of Wales Hospital, The Chinese University of Hong Kong, Hong Kong 999077, China.ORCID 0000-0002-4651-677X
Ka-Fai ToDepartment of Anatomical and Cellular Pathology, State Key Laboratory of Translational Oncology, Prince of Wales Hospital, The Chinese University of Hong Kong, Hong Kong 999077, China.
Hui-Yao LanLi Ka Shing Institute of Health Sciences, and Department of Medicine & Therapeutics, The Chinese University of Hong Kong, Hong Kong 999077, China.ORCID 0000-0003-4283-9755
Patrick Ming-Kuen TangDepartment of Anatomical and Cellular Pathology, State Key Laboratory of Translational Oncology, Prince of Wales Hospital, The Chinese University of Hong Kong, Hong Kong 999077, China.
Chinese University of Hong Kong · HKTongji University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Renal fibrosis is a common fate of chronic kidney diseases. Emerging studies suggest that unsolved inflammation will progressively transit into tissue fibrosis that finally results in an irreversible end-stage renal disease (ESRD). Renal inflammation recruits and activates immunocytes, which largely promotes tissue scarring of the diseased kidney. Importantly, studies have suggested a crucial role of innate immunity in the pathologic basis of kidney diseases. This review provides an update of both clinical and experimental information, focused on how innate immune signaling contributes to renal fibrogenesis. A better understanding of the underlying mechanisms may uncover a novel therapeutic strategy for ESRD.

Indexed as

Immunity, InnateAnimalsBiomarkersDisease SusceptibilityFibrosisHumansImmunosuppression TherapyMacrophagesMyofibroblastsRenal Insufficiency, ChronicSignal TransductionBiomarkerschronic kidney diseaseinflammationkidney fibrosismacrophage–myofibroblast transitionmicroenvironment

Identifiers

PMID32512831
PMCPMC7312694
OpenAlexW3034168062

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.