Evidence map›Paper›PMID 30674969›Full record

ArticleScientific reports2019

Astragaloside IV inhibits glucose-induced epithelial-mesenchymal transition of podocytes through autophagy enhancement via the SIRT-NF-κB p65 axis.

Xiaolei Wang, Yanbin Gao, Nianxiu Tian, Tao Wang, Yimin Shi, Jiayi Xu, Bingjie Wu

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
69citing papers in PubMed, 3 pooled it
10.5field-weighted citation impact, top 1% 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

69 citing papers in PubMed, 3 syntheses or guidelines pooled it, 109 citations in OpenAlex.

  1. Pooled it
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  4. Review
  5. Article
  6. Post‑translational modifications in diabetic kidney disease (Review).International journal of molecular medicine · 2026
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  18. Research Progress on the Anti-Cancer Effects ofMolecules (Basel, Switzerland) · 2024
    Review
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9 more citing papers are in PubMed but not listed here.

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

7 authors at 2 institutions in 1 country.

Xiaolei WangSchool of Traditional Chinese Medicine, Capital Medical University, 10 Youanmenwai, Xitoutiao, Fengtai District, Beijing, China.
Yanbin GaoSchool of Traditional Chinese Medicine, Capital Medical University, 10 Youanmenwai, Xitoutiao, Fengtai District, Beijing, China. dfyynfm@163.com.
Nianxiu TianSchool of Traditional Chinese Medicine, Capital Medical University, 10 Youanmenwai, Xitoutiao, Fengtai District, Beijing, China.
Tao WangSchool of Traditional Chinese Medicine, Capital Medical University, 10 Youanmenwai, Xitoutiao, Fengtai District, Beijing, China.
Yimin ShiBeijing Key Lab of TCM Collateral Disease theory Research, 10 Youanmenwai, Xitoutiao, Fengtai District, Beijing, China.
Jiayi XuSchool of Traditional Chinese Medicine, Capital Medical University, 10 Youanmenwai, Xitoutiao, Fengtai District, Beijing, China.
Bingjie WuSchool of Traditional Chinese Medicine, Capital Medical University, 10 Youanmenwai, Xitoutiao, Fengtai District, Beijing, China.
Capital Medical University · CNBeijing Fengtai Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Both autophagy and podocyte epithelial-mesenchymal transition (EMT) are critical factors in glomerular diseases that involve proteinuria and fibrosis. Here, we sought to determine whether plant-derived saponin astragaloside IV (AS-IV) was able to reverse renal fibrosis and improve renal function through regulation of autophagy and podocyte EMT. Cultured immortalized mouse podocytes and KK-Ay mice models of diabetes were exposed to AS-IV. Western blotting, real-time PCR, immunofluorescence and histochemistry were used to analyze markers of autophagy and podocyte EMT. We observed that AS-IV inhibited glucose-induced podocyte EMT and enhanced autophagy by decreasing NF-κB subunit p65 acetylation as well as increasing Sirtuin1 (SIRT1) expression. Treatment of the cells and animal models with a SIRT1 inhibitor EX527 was able to reverse these effects. The SIRT1 activator SRT1720 was also found to decrease p65 acetylation and enhance autophagy in glucose-induced podocyte EMT. Additionally, further treatment with autophagy inhibitor 3-methyladenine was able to reverse the effects of AS-IV on podocyte EMT, while the autophagy activator rapamycin or the NF-κB pathway inhibitor ammonium pyrrolidinedithiocarbamate (PDTC) were able to reverse glucose-induced podocyte EMT. Notably, both renal fibrosis and renal function in diabetic KK-Ay mice were improved after treatment with AS-IV. These findings support AS-IV as a renoprotective agent that likely exerts its effects on podocyte EMT through modulation of the SIRT1-NF-κB pathway and autophagy activation. Further studies are required to clarify the role of AS-IV as a potential therapeutic agent in glomerular diseases.

Indexed as

AutophagyAnimalsCell LineDiabetic NephropathiesDisease Models, AnimalEpithelial-Mesenchymal TransitionGlucoseKidney Function TestsMiceModels, BiologicalPodocytesSaponinsSirtuin 1Transcription Factor RelATreatment OutcomeTriterpenesastragaloside AGlucoseRela protein, mouseSaponinsSirt1 protein, mouseSirtuin 1Transcription Factor RelATriterpenes

Identifiers

PMID30674969
PMCPMC6344540
OpenAlexW2913166170

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.