Evidence map›Paper›PMID 30604228›Full record

ArticleInternational urology and nephrology2019

Aspirin attenuates podocyte injury in diabetic rats through overriding cyclooxygenase-2-mediated dysregulation of LDL receptor pathway.

Kun Ling Ma, Liang Liu, Yang Zhang, Gui Hua Wang, Ze Bo Hu, Pei Pei Chen, Jian Lu, Chen Chen Lu, Tie Kai Gong, Yu Xiang Gong and 1 more

Abstract read
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In one paragraph

Article in International urology and nephrology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.7field-weighted citation impact, top 32% 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

5 citing papers in PubMed, 7 citations in OpenAlex.

  1. Review
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  4. Mechanism ofFrontiers in pharmacology · 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

11 authors at 1 institution in 1 country.

Kun Ling MaInstitute of Nephrology, Zhong Da Hospital, Medical School of Southeast University, NO. 87, Ding Jia Qiao Road, Nang Jing, 210009, Jiang Su, China. klma05@163.com.ORCID http://orcid.org/0000-0001-9238-2867
Liang LiuInstitute of Nephrology, Zhong Da Hospital, Medical School of Southeast University, NO. 87, Ding Jia Qiao Road, Nang Jing, 210009, Jiang Su, China.
Yang ZhangInstitute of Nephrology, Zhong Da Hospital, Medical School of Southeast University, NO. 87, Ding Jia Qiao Road, Nang Jing, 210009, Jiang Su, China.
Gui Hua WangInstitute of Nephrology, Zhong Da Hospital, Medical School of Southeast University, NO. 87, Ding Jia Qiao Road, Nang Jing, 210009, Jiang Su, China.
Ze Bo HuInstitute of Nephrology, Zhong Da Hospital, Medical School of Southeast University, NO. 87, Ding Jia Qiao Road, Nang Jing, 210009, Jiang Su, China.
Pei Pei ChenInstitute of Nephrology, Zhong Da Hospital, Medical School of Southeast University, NO. 87, Ding Jia Qiao Road, Nang Jing, 210009, Jiang Su, China.
Jian LuInstitute of Nephrology, Zhong Da Hospital, Medical School of Southeast University, NO. 87, Ding Jia Qiao Road, Nang Jing, 210009, Jiang Su, China.
Chen Chen LuInstitute of Nephrology, Zhong Da Hospital, Medical School of Southeast University, NO. 87, Ding Jia Qiao Road, Nang Jing, 210009, Jiang Su, China.
Tie Kai GongInstitute of Nephrology, Zhong Da Hospital, Medical School of Southeast University, NO. 87, Ding Jia Qiao Road, Nang Jing, 210009, Jiang Su, China.
Yu Xiang GongInstitute of Nephrology, Zhong Da Hospital, Medical School of Southeast University, NO. 87, Ding Jia Qiao Road, Nang Jing, 210009, Jiang Su, China.
Bi Cheng LiuInstitute of Nephrology, Zhong Da Hospital, Medical School of Southeast University, NO. 87, Ding Jia Qiao Road, Nang Jing, 210009, Jiang Su, China.
Zhongda Hospital Southeast University · CN

Funding

the Fundamental Research Funds for the Central Universities KYCX17-0169the Fundamental Research Funds for the Central Universities KYCX18-0182the Fundamental Research Funds for the Central Universities KYZZ15-0061the Jiangsu Province Ordinary University Graduate Research Innovation Project SJZZ16-004the Jiangsu Province Six Talent Peaks Project 2015-WSN-002the Jiangsu Province Social Development Project BE2018744the National Natural Science Foundation of China 81470957the Project for Jiangsu Provincial Medical Talent ZDRCA2016077the Project of Nanjing Municipal Committee for Health and Family Planning YKK17280
6 · The paper itself

Abstract

aimThis study aimed to investigate the effects of aspirin on podocyte injury and its underlying mechanisms in diabetic nephropathy (DN).

methodsEight-week-old male Sprague-Dawley rats were divided into three groups: non-diabetic rats (Control), streptozotocin-induced diabetic rats (DM), and diabetic rats treated with aspirin (DM + Aspirin) for 12 weeks. Intracellular lipid accumulation was evaluated by Oil Red O staining and quantitative free cholesterol assays. Podocyte injury and the levels of COX-2, inflammatory cytokines, and low-density lipoprotein receptor (LDLr) pathway-related proteins were evaluated by electron microscopy, immunohistochemical staining, and Western blotting, respectively.

resultsLipid levels and urinary albumin-creatinine ratios were higher in the DM rats than in the Control rats. Periodic acid-Schiff staining showed glomerular hypertrophy and mild mesangial area widening in the DM rats. Electron microscopy showed that the podocyte foot processes were significantly flattened or absent in the DM rats. The protein expression levels of WT-1 and nephrin in the podocytes of DM rats were reduced. Interestingly, lipid accumulation in the kidneys of DM rats was significantly increased due to increased protein expression levels of LDLr, sterol regulatory element-binding protein (SREBP) cleavage-activating protein (SCAP), SREBP-2, cyclooxygenase-2 (COX-2), and inflammatory cytokines. Confocal immunofluorescent staining showed that COX-2 and WT-1 were co-expressed. Furthermore, COX-2 protein expression levels were positively correlated with LDLr protein expression levels. However, when COX-2 expression was inhibited by aspirin, these changes in the DM rats were significantly attenuated.

conclusionAspirin attenuates podocyte injury in DN, which may be through COX-2-mediated dysregulation of LDLr pathway.

Indexed as

AlbuminuriaAnimalsAspirinCreatinineCyclooxygenase 2Cyclooxygenase 2 InhibitorsCytokinesDiabetes Mellitus, ExperimentalGlomerular MesangiumHypertrophyMaleMembrane ProteinsPodocytesRatsRats, Sprague-DawleyReceptors, LDLAspirinCreatinineCyclooxygenase 2Cyclooxygenase 2 InhibitorsCytokinesMembrane ProteinsnephrinReceptors, LDLSrebf2 protein, ratSterol Regulatory Element Binding ProteinsWt1 protein, ratWT1 ProteinsAspirinCyclooxygenase-2Diabetic nephropathyLDL receptorPodocyte injury

Identifiers

PMID30604228
OpenAlexW2907901828

What OpenQuestion holds

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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.