Evidence map›Paper›PMID 30863013›Full record

ArticleDrug design, development and therapy2019

Maresin 1 mitigates renal ischemia/reperfusion injury in mice via inhibition of the TLR4/MAPK/NF-κB pathways and activation of the Nrf2 pathway.

Yun Qiu, Yichen Wu, Hongmei Zhao, Hong Sun, Sumin Gao

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

Article in Drug design, development and therapy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed, 2 pooled it
6.1field-weighted citation impact, top 3% 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

40 citing papers in PubMed, 2 syntheses or guidelines pooled it, 76 citations in OpenAlex.

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  7. Maresins.Biomolecules · 2026
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  17. [Maresin1 inhibits the NF-κB/caspase-3/GSDME signaling pathway to alleviate hepatic ischemia-reperfusion injury].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2023
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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

5 authors at 1 institution in 1 country.

Yun QiuDepartment of Emergency Medicine, The Affiliated Huaian No 1 People's Hospital of Nanjing Medical University, Huai'an, Jiangsu Province, China, gao666332@sina.com.
Yichen WuDepartment of Emergency Medicine, The Affiliated Huaian No 1 People's Hospital of Nanjing Medical University, Huai'an, Jiangsu Province, China, gao666332@sina.com.
Hongmei ZhaoDepartment of Emergency Medicine, The Affiliated Huaian No 1 People's Hospital of Nanjing Medical University, Huai'an, Jiangsu Province, China, gao666332@sina.com.
Hong SunDepartment of Emergency Medicine, The Affiliated Huaian No 1 People's Hospital of Nanjing Medical University, Huai'an, Jiangsu Province, China, gao666332@sina.com.
Sumin GaoDepartment of Emergency Medicine, The Affiliated Huaian No 1 People's Hospital of Nanjing Medical University, Huai'an, Jiangsu Province, China, gao666332@sina.com.
Xuzhou Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundInflammation and oxidative stress play a crucial role in the pathogenesis of renal ischemia/reperfusion injury (IRI). Maresin 1 (MaR1), which has shown strong anti-inflammatory and antioxidant effects, was recently reported to have protective properties in several different animal models.

aimThe objectives of our study were to determine whether MaR1 alleviates renal IRI and to identify the underlying mechanisms. MATERIALS AND

methodsThe mouse model in this study was induced by ischemia of the left kidney for 45 minutes and by nephrectomy of the right kidney. All mice were intravenously injected with a vehicle or MaR1. Renal histopathologic changes, function, proinflammatory cytokines, and oxidative stress were assessed. The expression of proteins was measured by Western blot.

resultsThe results indicated that MaR1 markedly protected against renal IRI. The protective effects were accompanied by the reduction of histologic changes and reduction of renal dysfunction. Meanwhile, MaR1 remarkably mitigated renal IRI-induced inflammation and oxidative stress. In addition, our results showed that MaR1 significantly inhibited the expression of TLR4 and the expression of phosphorylated Erk, JNK, and P38. Furthermore, MaR1 decreased the nuclear translocation of NF-κB and increased the nuclear translocation of Nrf2.

conclusionMaR1 protects against renal IRI by inhibiting the TLR4/MAPK/NF-κB pathways, which mediate anti-inflammation, and by activating the Nrf2 pathway, which mediates antioxidation.

Indexed as

AnimalsAnti-Inflammatory AgentsDisease Models, AnimalDocosahexaenoic AcidsKidney DiseasesMaleMAP Kinase Signaling SystemMiceMice, Inbred C57BLMitogen-Activated Protein KinasesNF-E2-Related Factor 2NF-kappa BOxidative StressReperfusion InjuryToll-Like Receptor 47,14-dihydroxydocosa-4,8,10,12,16,19-hexaenoic acidAnti-Inflammatory AgentsDocosahexaenoic AcidsMitogen-Activated Protein KinasesNfe2l2 protein, mouseNF-E2-Related Factor 2NF-kappa BTlr4 protein, mouseToll-Like Receptor 4MAPKMaresin 1NF-κBNrf2renal ischemia/reperfusion injuryTLR4

Identifiers

PMID30863013
PMCPMC6388965
OpenAlexW2915512246

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.