Evidence map›Paper›PMID 29999001›Full record

ArticleMedical science monitor : international medical journal of experimental and clinical research2018

Genistein and Myd88 Activate Autophagy in High Glucose-Induced Renal Podocytes In Vitro.

Yuanyuan Wang, Ying Li, Tao Zhang, Yanqing Chi, Maodong Liu, Ying Liu

Open access · bronzeAbstract read
In one paragraph

Article in Medical science monitor : international medical journal of experimental and clinical research, 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
2.4field-weighted citation impact, top 11% 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, 32 citations in OpenAlex.

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  18. Toll-Like Receptor as a Potential Biomarker in Renal Diseases.International journal of molecular sciences · 2020
    Review
  19. Genistein Induces Adipogenic and Autophagic Effects in Rainbow Trout (International journal of molecular sciences · 2020
    Article
  20. Morroniside Inhibits HFrontiers in pharmacology · 2020
    Article
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

6 authors at 2 institutions in 1 country.

Yuanyuan WangDepartment of Nephrology, Hebei Medical University Third Affiliated Hospital, Shijiazhuang, Hebei, China (mainland).
Ying LiDepartment of Nephrology, Hebei Medical University Third Affiliated Hospital, Shijiazhuang, Hebei, China (mainland).
Tao ZhangDepartment of Nephrology, Hebei Medical University Third Affiliated Hospital, Shijiazhuang, Hebei, China (mainland).
Yanqing ChiDepartment of Nephrology, Hebei Medical University Third Affiliated Hospital, Shijiazhuang, Hebei, China (mainland).
Maodong LiuDepartment of Nephrology, Hebei Medical University Third Affiliated Hospital, Shijiazhuang, Hebei, China (mainland).
Ying LiuDepartment of Science and Education, North China University of Science and Technology Affiliated Hospital, Tangshan, Hebei, China (mainland).
Third Hospital of Hebei Medical University · CNNorth China University of Science and Technology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND Renal podocyte damage plays a crucial role in the development of diabetic nephropathy. Genistein is derived from a leguminous plant, and MyD88 and TRIF are adaptor molecules in the Toll-like receptor (TLR) signaling pathway, which may play a role in autophagy. In this study, we utilized an in vitro high glucose (HG)-treated podocyte model to investigate the effects and underlying mechanisms of Genistein and MyD88 or TRIF siRNA induced autophagy and renal protection. MATERIAL AND METHODS An immortalized mouse podocyte cell line was treated with HG, Genistein, chloroquine, and/or transfected with specific Myd88 and TRIF siRNAs. The formation of autophagosomes and related autophagic vacuoles were monitored by transmission electron microscopy. The expression of autophagy-related factors and podocyte structure and functional markers, including LC3, p62, p-mTOR, synaptopodin, and nephrin, were measured by Western blot, and LC3 and p-mTOR expression were also assessed by immunofluorescence. RESULTS We showed that HG transiently (after 6-h exposure) induced expression of the autophagy activation marker LC3-II in podocytes. Genistein treatment induced autophagy in both normal and HG-treated podocytes through inactivating mTOR signaling. Moreover, Genistein protected podocytes against chloroquine in HG-cultured conditions in vitro by maintaining the level of autophagy-related proteins. In addition, MyD88 siRNA downregulated expression of autophagy-related proteins, whereas Genistein treatment reversed these effects. CONCLUSIONS This study demonstrated that Genistein-induced autophagy could be a potential treatment strategy for glomerular diseases.

Indexed as

Adaptor Proteins, Vesicular TransportAnimalsAutophagyCell LineChloroquineGenisteinGlucoseMiceMicrotubule-Associated ProteinsMyeloid Differentiation Factor 88PodocytesSignal TransductionTOR Serine-Threonine KinasesAdaptor Proteins, Vesicular TransportChloroquineGenisteinGlucoseMap1lc3b protein, mouseMicrotubule-Associated ProteinsMyeloid Differentiation Factor 88Ticam1 protein, mouseTOR Serine-Threonine Kinases

Identifiers

PMID29999001
PMCPMC6069420
OpenAlexW2854408917

What OpenQuestion holds

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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.