Evidence map›Paper›PMID 29621130›Full record

ArticleMarine drugs2018

Astaxanthin Promotes Nrf2/ARE Signaling to Inhibit HG-Induced Renal Fibrosis in GMCs.

Xi Xie, Qing Chen, Jun Tao

Open access · goldAbstract read
In one paragraph

Article in Marine drugs, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
4.3field-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

35 citing papers in PubMed, 68 citations in OpenAlex.

  1. Review
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  12. Mitochondrial Pathophysiology on Chronic Kidney Disease.International journal of molecular sciences · 2022
    Review
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  15. Article
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  18. Article
  19. The Promising Effects of Astaxanthin on Lung Diseases.Advances in nutrition (Bethesda, Md.) · 2021
    Review
  20. Review
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

3 authors at 1 institution in 1 country.

Xi XieKey Laboratory of Tropical Biological Resources of Ministry of Education, Hainan University, Haikou 570228, China. xiexi@hainu.edu.cn.
Qing ChenHainan Key Laboratory of Sustainable Utilization of Tropical Bioresources, Hainan University, Haikou 570228, China. chenqing1984@hainu.edu.cn.
Jun TaoHainan Key Laboratory of Sustainable Utilization of Tropical Bioresources, Hainan University, Haikou 570228, China. taoj@hainu.edu.cn.ORCID 0000-0002-9046-0283
Hainan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Oxidative stress is the main cause of diabetic nephropathy (DN) progression. Nuclear factor-erythroid 2-related factor 2 (Nrf2)/antioxidant response element (ARE) signaling is a crucial cellular defense system to cope with oxidative stress. Astaxanthin (AST) is a fat-soluble xanthophyll carotenoid with remarkable antioxidative capacity. AST exerted renal protective in diabetic rats. This study aimed to determine whether AST could alleviate the pathological progress of DN by activating Nrf2/ARE signaling and diminishing the excessive oxidative stress and fibronectin (FN) accumulation in glomerular mesangial cells (GMCs) challenged with high glucose (HG). In the current study, we found that AST treatment alleviated the metabolic parameters, renal morphology and extracellular matrix (ECM) accumulation in streptozotocin-induced diabetic rats. Additionally, HG induced the adaptively activated Nrf2/ARE signaling and increased the expression of FN, intercellular adhesion molecule-1 (ICAM-1) and transforming growth factor-β1 (TGF-β1), as well as the intracellular reactive oxygen species (ROS) generation in GMCs. However, AST treatment strongly promoted the nuclear translocation and transcriptional activity of Nrf2 as well as upregulated the expression of superoxide dismutase (SOD1), NAD(P)H: quinone oxidoreductase (NQO1) and heme oxygenase-1 (HO-1), ultimately quenching the higher level of ROS and inhibiting the FN, ICAM-1 and TGF-β1 expression induced by HG. Collectively, our data suggest that the renoprotective effect of AST on DN depends on Nrf2/ARE signaling activation, which could be a potentially therapeutic strategy in the treatment of DN.

Indexed as

AnimalsAntioxidant Response ElementsCells, CulturedDiabetes Mellitus, ExperimentalDiabetic NephropathiesExtracellular MatrixFibrinolytic AgentsFibronectinsFibrosisGlucoseHumansMaleMesangial CellsNF-E2-Related Factor 2Oxidative StressRatsastaxanthineFibrinolytic AgentsFibronectinsGlucoseNfe2l2 protein, ratNF-E2-Related Factor 2StreptozocinXanthophyllsastaxanthindiabetic nephropathyNrf2/ARE signalingoxidative stressrenal fibrosis

Identifiers

PMID29621130
PMCPMC5923404
OpenAlexW2795635674

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.