Evidence mapPaperPMID 30185654Full record

ArticleJCI insight2018

Lipocalin-2 derived from adipose tissue mediates aldosterone-induced renal injury.

Wai Yan Sun, Bo Bai, Cuiting Luo, Kangmin Yang, Dahui Li, Donghai Wu, Michel Félétou, Nicole Villeneuve, Yang Zhou, Junwei Yang and 3 more

Open access · goldAbstract read
In one paragraph

Article in JCI insight, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.6field-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

22 citing papers in PubMed, 48 citations in OpenAlex.

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  14. Mechanisms of Post-critical Illness Cardiovascular Disease.Frontiers in cardiovascular medicine · 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

13 authors at 4 institutions in 4 countries.

Wai Yan SunThe State Key Laboratory of Pharmaceutical Biotechnology and.
Bo BaiThe State Key Laboratory of Pharmaceutical Biotechnology and.
Cuiting LuoThe State Key Laboratory of Pharmaceutical Biotechnology and.
Kangmin YangThe State Key Laboratory of Pharmaceutical Biotechnology and.
Dahui LiThe State Key Laboratory of Pharmaceutical Biotechnology and.
Donghai WuKey Laboratory of Regenerative Biology, Guangzhou Institute of Biomedicine and Health, Chinese Academy of Sciences, Guangzhou, China.
Michel FélétouThe Institut de Recherches Servier, Suresnes, France.
Nicole VilleneuveThe Institut de Recherches Servier, Suresnes, France.
Yang ZhouCenter for Kidney Disease, Second Affiliated Hospital, Nanjing Medical University, China.
Junwei YangCenter for Kidney Disease, Second Affiliated Hospital, Nanjing Medical University, China.
Aimin XuThe State Key Laboratory of Pharmaceutical Biotechnology and.
Paul M VanhoutteThe State Key Laboratory of Pharmaceutical Biotechnology and.
Yu WangThe State Key Laboratory of Pharmaceutical Biotechnology and.
Pharmaceutical Biotechnology (Czechia) · CZSecond Affiliated Hospital of Nanjing Medical University · CNServier (France) · FRChinese Academy of Sciences · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lipocalin-2 is not only a sensitive biomarker, but it also contributes to the pathogenesis of renal injuries. The present study demonstrates that adipose tissue-derived lipocalin-2 plays a critical role in causing both chronic and acute renal injuries. Four-week treatment with aldosterone and high salt after uninephrectomy (ANS) significantly increased both circulating and urinary lipocalin-2, and it induced glomerular and tubular injuries in kidneys of WT mice. Despite increased renal expression of lcn2 and urinary excretion of lipocalin-2, mice with selective deletion of lcn2 alleles in adipose tissue (Adipo-LKO) are protected from ANS- or aldosterone-induced renal injuries. By contrast, selective deletion of lcn2 alleles in kidney did not prevent aldosterone- or ANS-induced renal injuries. Transplantation of fat pads from WT donors increased the sensitivity of mice with complete deletion of Lcn2 alleles (LKO) to aldosterone-induced renal injuries. Aldosterone promoted the urinary excretion of a human lipocalin-2 variant, R81E, in turn causing renal injuries in LKO mice. Chronic treatment with R81E triggered significant renal injuries in LKO, resembling those observed in WT mice following ANS challenge. Taken in conjunction, the present results demonstrate that lipocalin-2 derived from adipose tissue causes acute and chronic renal injuries, largely independent of local lcn2 expression in kidney.

Indexed as

Acute Kidney InjuryAdipose TissueAldosteroneAllelesAnimalsBiomarkersDisease Models, AnimalFemaleFibrosisHumansKidneyLipocalin-2MaleMiceMice, Inbred C57BLMice, KnockoutAldosteroneBiomarkersLCN2 protein, humanLcn2 protein, mouseLipocalin-2Recombinant ProteinsAdipose tissueInflammationMouse modelsNephrology

Identifiers

PMID30185654
PMCPMC6171815
OpenAlexW2892204031

What Socratic 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 Socratic graph.