Evidence map›Paper›PMID 26733332›Full record

ArticleJournal of nephrology2016

Metformin modulates apoptosis and cell signaling of human podocytes under high glucose conditions.

Sebastian Langer, Reinhold Kreutz, Andreas Eisenreich

Abstract read
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In one paragraph

Article in Journal of nephrology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 1 pooled it
5.7field-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

28 citing papers in PubMed, 1 synthesis or guideline pooled it, 61 citations in OpenAlex.

  1. Pooled it
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  14. Accelerated Kidney Aging in Diabetes Mellitus.Oxidative medicine and cellular longevity · 2020
    Review
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  18. Metformin increases glucose uptake and acts renoprotectively by reducing SHIP2 activity.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019
    Article
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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

3 authors at 1 institution in 1 country.

Sebastian LangerKlinische Pharmakologie und Toxikologie, CC04, Charité-Universitätsmedizin Berlin, Charitéplatz 1, 10117, Berlin, Germany.
Reinhold KreutzKlinische Pharmakologie und Toxikologie, CC04, Charité-Universitätsmedizin Berlin, Charitéplatz 1, 10117, Berlin, Germany.
Andreas EisenreichKlinische Pharmakologie und Toxikologie, CC04, Charité-Universitätsmedizin Berlin, Charitéplatz 1, 10117, Berlin, Germany. andreas.eisenreich@charite.de.
Charité - Universitätsmedizin Berlin · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diabetic nephropathy, which is associated with loss of human (h) podocytes (PC), is a major complication in diabetes mellitus. High-glucose modulates AMP-activated protein kinase (AMPK) signaling and cell apoptosis. Metformin has been demonstrated to reduce apoptosis and albuminuria in type 2 diabetes. Here, we examined the effect of metformin on cell apoptosis and on pro-/anti-apoptotic signaling in hPC. Expression analyses were done by real-time polymerase chain reaction and western blotting. Moreover, a functional apoptosis assay was performed in hPC. Determination of kinase activation by phosphorylation was done via immunodetection analyses and digital quantification. We found that hPC express organic cation transporter 1 which is the major uptake transporter of metformin. High-glucose reduced AMPK phosphorylation and induced mammalian target of rapamycin (mTOR) activation in podocytes, which was abolished and reversed by pre-treatment with metformin. Furthermore, metformin reduced high-glucose-induced podocytes apoptosis in a concentration-dependent manner. In summary, metformin exhibits an anti-apoptotic impact on podocytes under high-glucose conditions via activation of AMPK and inhibition of mTOR signaling. These data support a beneficial effect of metformin in diabetic nephropathy.

Indexed as

AMP-Activated Protein KinasesApoptosisCell LineCell SurvivalCytoprotectionDiabetic NephropathiesDose-Response Relationship, DrugGlucoseHumansHypoglycemic AgentsMetforminOrganic Cation Transporter 1PhosphorylationPodocytesSignal TransductionTOR Serine-Threonine KinasesAMP-Activated Protein KinasesGlucoseHypoglycemic AgentsMetforminMTOR protein, humanOrganic Cation Transporter 1TOR Serine-Threonine KinasesApoptosisDiabetic nephropathyGlucosePodocytes

Identifiers

PMID26733332
OpenAlexW2222574236

What OpenQuestion holds

Texttitle and abstract
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.