Evidence map›Paper›PMID 28112381›Full record

ArticleInternational journal of molecular medicine2017

Notoginsenoside R1 attenuates glucose-induced podocyte injury via the inhibition of apoptosis and the activation of autophagy through the PI3K/Akt/mTOR signaling pathway.

Guodong Huang, Bingyu Zou, Jianzhen Lv, Tongyu Li, Guoli Huai, Shaowei Xiang, Shilong Lu, Huan Luo, Yaping Zhang, Yi Jin and 1 more

Open access · hybridAbstract read
In one paragraph

Article in International journal of molecular medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

23 citing papers in PubMed, 43 citations in OpenAlex.

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  18. Calpain-10 drives podocyte apoptosis and renal injury in diabetic nephropathy.Diabetes, metabolic syndrome and obesity : targets and therapy · 2019
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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 5 institutions in 2 countries.

Guodong HuangDepartment of Nephrology, Ruikang Hospital Affiliated to Guangxi University of Chinese Medicine, Nanning, Guangxi 530011, P.R. China.
Bingyu ZouDepartment of Gynecology, Sichuan Academy of Medical Science and Sichuan Provincial People's Hospital, Chengdu, Sichuan 610072, P.R. China.
Jianzhen LvSchool of Basic Medical Science, Guangxi University of Chinese Medicine, Nanning, Guangxi 530001, P.R. China.
Tongyu LiSchool of Basic Medical Science, Guangxi University of Chinese Medicine, Nanning, Guangxi 530001, P.R. China.
Guoli HuaiDepartment of Biomedical Engineering, Medical School of University of Electronic Science and Technology of China, Chengdu, Sichuan 610054, P.R. China.
Shaowei XiangDepartment of Nephrology, Ruikang Hospital Affiliated to Guangxi University of Chinese Medicine, Nanning, Guangxi 530011, P.R. China.
Shilong LuSchool of Basic Medical Science, Guangxi University of Chinese Medicine, Nanning, Guangxi 530001, P.R. China.
Huan LuoDepartment of Nephrology, Ruikang Hospital Affiliated to Guangxi University of Chinese Medicine, Nanning, Guangxi 530011, P.R. China.
Yaping ZhangDepartment of Nephrology, Ruikang Hospital Affiliated to Guangxi University of Chinese Medicine, Nanning, Guangxi 530011, P.R. China.
Yi JinCenter for Perinatal Research, Research Institute at Nationwide Children's Hospital, Columbus, OH 43215, USA.
Yi WangDepartment of Biomedical Engineering, Medical School of University of Electronic Science and Technology of China, Chengdu, Sichuan 610054, P.R. China.
Guangxi University of Chinese Medicine · CNGuangxi University · CNUniversity of Electronic Science and Technology of China · CNNationwide Children's Hospital · USSichuan Academy of Medical Sciences & Sichuan Provincial People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Injury to terminally differentiated podocytes contributes ignificantly to proteinuria and glomerulosclerosis. The aim of this study was to examine the protective effects of notoginsenoside R1 (NR1) on the maintenance of podocyte number and foot process architecture via the inhibition of apoptosis, the induction of autophagy and the maintenance pf podocyte biology in target cells. The effects of NR1 on conditionally immortalized human podocytes under high glucose conditions were evaluated by determining the percentage apoptosis, the percentage autophagy and the expression levels of slit diaphragm proteins. Our results revealed that NR1 protected the podocytes against high glucose-induced injury by decreasing apoptosis, increasing autophagy and by promoting cytoskeletal recovery. The phosphoinositide 3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) signaling pathway was further investigated in order to elucidate the mechanisms responsible for the protective effects of NR1 on podocytes. Our data indicated that treatment with NR increased the phosphorylation levels of PI3K, Akt and mTOR, leading to the activation of the PI3K/Akt/mTOR signaling pathway in podocytes. To the best of our knowledge, this is the first in vitro study to demonstrate that NR1 protects podocytes by activating the PI3K/Akt/mTOR pathway.

Indexed as

Signal TransductionApoptosisBiomarkersCell LineGene ExpressionGinsenosidesGlucoseHumansPhosphatidylinositol 3-KinasesPodocytesProto-Oncogene Proteins c-aktTOR Serine-Threonine KinasesBiomarkersGinsenosidesGlucosenotoginsenoside R1Phosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktTOR Serine-Threonine Kinases

Identifiers

PMID28112381
PMCPMC5360354
OpenAlexW2579790707

What OpenQuestion holds

Textmetadata
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.