Evidence map›Paper›PMID 31942046›Full record

ReviewNature reviews. Nephrology2020

Innate immunity in diabetic kidney disease.

Sydney C W Tang, Wai Han Yiu

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Nephrology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 384 papers, 6 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
384citing papers in PubMed, 6 pooled it
40.9field-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

384 citing papers in PubMed, 6 syntheses or guidelines pooled it, 574 citations in OpenAlex.

  1. Pooled it
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  13. Disulfiram Attenuates Adenine-Induced Renal Fibrosis by Modulating Inflammatory and Immunometabolic Responses.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
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  14. Review
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  17. CCL5 mRNA-enriched small extracellular vesicles from renal tubular epithelial cells enhance macrophage inflammatory responses in diabetic nephropathy.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Article
  18. Article
  19. Article
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324 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 2 countries.

Sydney C W TangDivision of Nephrology, Department of Medicine, The University of Hong Kong, Queen Mary Hospital, Hong Kong, China. scwtang@hku.hk.ORCID http://orcid.org/0000-0002-6862-1941
Wai Han YiuDivision of Nephrology, Department of Medicine, The University of Hong Kong, Queen Mary Hospital, Hong Kong, China.
Queen Mary Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Increasing evidence suggests that renal inflammation contributes to the pathogenesis and progression of diabetic kidney disease (DKD) and that anti-inflammatory therapies might have renoprotective effects in DKD. Immune cells and resident renal cells that activate innate immunity have critical roles in triggering and sustaining inflammation in this setting. Evidence from clinical and experimental studies suggests that several innate immune pathways have potential roles in the pathogenesis and progression of DKD. Toll-like receptors detect endogenous danger-associated molecular patterns generated during diabetes and induce a sterile tubulointerstitial inflammatory response via the NF-κB signalling pathway. The NLRP3 inflammasome links sensing of metabolic stress in the diabetic kidney to activation of pro-inflammatory cascades via the induction of IL-1β and IL-18. The kallikrein-kinin system promotes inflammatory processes via the generation of bradykinins and the activation of bradykinin receptors, and activation of protease-activated receptors on kidney cells by coagulation enzymes contributes to renal inflammation and fibrosis in DKD. In addition, hyperglycaemia leads to protein glycation and activation of the complement cascade via recognition of glycated proteins by mannan-binding lectin and/or dysfunction of glycated complement regulatory proteins. Data from preclinical studies suggest that targeting these innate immune pathways could lead to novel therapies for DKD.

Indexed as

AnimalsDiabetes MellitusDiabetic NephropathiesDisease ProgressionFemaleHumansImmunity, InnateInflammasomesMaleMicePrognosisRisk AssessmentSeverity of Illness IndexSurvival AnalysisToll-Like ReceptorsInflammasomesToll-Like Receptors

Identifiers

PMID31942046
OpenAlexW2999140222

What OpenQuestion holds

Textmetadata
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.