Evidence map›Paper›PMID 28623824›Full record

ArticleRedox biology2017

Dietary nitrate attenuates renal ischemia-reperfusion injuries by modulation of immune responses and reduction of oxidative stress.

Ting Yang, Xing-Mei Zhang, Laura Tarnawski, Maria Peleli, Zhengbing Zhuge, Niccolo Terrando, Robert A Harris, Peder S Olofsson, Erik Larsson, A Erik G Persson and 3 more

Open access · goldAbstract read
In one paragraph

Article in Redox biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
5.1field-weighted citation impact, top 4% 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

33 citing papers in PubMed, 79 citations in OpenAlex.

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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 3 institutions in 2 countries.

Ting YangDept. of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden; Dept. of Medicine, Div. of Nephrology (T.Y.), Dept. of Anesthesiology (N.T.), Duke University Medical Center, Durham, NC, USA. Electronic address: ting.yang2@duke.edu.
Xing-Mei ZhangDept. of Clinical Neuroscience, Karolinska Institutet, Center for Molecular Medicine, Karolinska University Hospital Solna, Stockholm, Sweden.
Laura TarnawskiDept. of Medicine, Center for Molecular Medicine, Solna, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden.
Maria PeleliDept. of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
Zhengbing ZhugeDept. of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
Niccolo TerrandoDept. of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden; Dept. of Medicine, Div. of Nephrology (T.Y.), Dept. of Anesthesiology (N.T.), Duke University Medical Center, Durham, NC, USA.
Robert A HarrisDept. of Clinical Neuroscience, Karolinska Institutet, Center for Molecular Medicine, Karolinska University Hospital Solna, Stockholm, Sweden.
Peder S OlofssonDept. of Medicine, Center for Molecular Medicine, Solna, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden.
Erik LarssonDept. of Immunology, Genetics and Pathology, Uppsala University, Sweden.
A Erik G PerssonDept. of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden; Dept. of Medical Cell Biology, Uppsala University, Sweden.
Jon O LundbergDept. of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
Eddie WeitzbergDept. of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
Mattias CarlstromDept. of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden. Electronic address: mattias.carlstrom@ki.se.
Karolinska Institutet · SEKarolinska University Hospital · SEUppsala University · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ischemia-reperfusion (IR) injury involves complex pathological processes in which reduction of nitric oxide (NO) bioavailability is suggested as a key factor. Inorganic nitrate can form NO in vivo via NO synthase-independent pathways and may thus provide beneficial effects during IR. Herein we evaluated the effects of dietary nitrate supplementation in a renal IR model. Male mice (C57BL/6J) were fed nitrate-supplemented chow (1.0mmol/kg/day) or standard chow for two weeks prior to 30min ischemia and during the reperfusion period. Unilateral renal IR caused profound tubular and glomerular damage in the ischemic kidney. Renal function, assessed by plasma creatinine levels, glomerular filtration rate and renal plasma flow, was also impaired after IR. All these pathologies were significantly improved by nitrate. Mechanistically, nitrate treatment reduced renal superoxide generation, pro-inflammatory cytokines (IL-1β, IL-6 and IL-12 p70) and macrophage infiltration in the kidney. Moreover, nitrate reduced mRNA expression of pro-inflammatory cytokines and chemo attractors, while increasing anti-inflammatory cytokines in the injured kidney. In another cohort of mice, two weeks of nitrate supplementation lowered superoxide generation and IL-6 expression in bone marrow-derived macrophages. Our study demonstrates protective effect of dietary nitrate in renal IR injury that may be mediated via modulation of oxidative stress and inflammatory responses. These novel findings suggest that nitrate supplementation deserve further exploration as a potential treatment in patients at high risk of renal IR injury.

Indexed as

Oxidative StressAcute Kidney InjuryAnimalsCells, CulturedDietary SupplementsInterleukin-6KidneyMacrophage ActivationMacrophagesMaleMiceMice, Inbred C57BLNitratesReperfusion InjurySuperoxidesInterleukin-6NitratesSuperoxidesAcute kidney injuryInflammationInorganic nitrateNADPH oxidaseNitric oxideOxidative stress

Identifiers

PMID28623824
PMCPMC5473548
OpenAlexW2621527552

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.