Evidence map›Paper›PMID 26103809›Full record

ArticleJournal of cellular and molecular medicine2015

Apelin promotes diabetic nephropathy by inducing podocyte dysfunction via inhibiting proteasome activities.

Caixia Guo, Yu Liu, Wenjie Zhao, Shengnan Wei, Xiaoli Zhang, Wenying Wang, Xiangjun Zeng

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of cellular and molecular medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
4.2field-weighted citation impact, top 6% 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

27 citing papers in PubMed, 44 citations in OpenAlex.

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  16. Impairment of Proteasome Function in Podocytes Leads to CKD.Journal of the American Society of Nephrology : JASN · 2021
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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

7 authors at 1 institution in 1 country.

Caixia GuoDepartment of Pathophysiology and Pathology, Capital Medical University, Beijing, China.
Yu LiuDepartment of Pathophysiology and Pathology, Capital Medical University, Beijing, China.
Wenjie ZhaoDepartment of Pathophysiology and Pathology, Capital Medical University, Beijing, China.
Shengnan WeiDepartment of Pathophysiology and Pathology, Capital Medical University, Beijing, China.
Xiaoli ZhangDepartment of Pathophysiology and Pathology, Capital Medical University, Beijing, China.
Wenying WangDepartment of Urology, Beijing Friendship Hospital, Capital Medical University, Beijing, China.
Xiangjun ZengDepartment of Pathophysiology and Pathology, Capital Medical University, Beijing, China.
Capital Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Podocyte injuries are associated with progression of diabetic nephropathy (DN). Apelin, an adipocyte-derived peptide, has been reported to be a promoting factor for DN. In this study, we aim to determine whether apelin promotes progression of DN by inducing podocyte dysfunction. kk-Ay mice were used as models for DN. Apelin and its antagonist, F13A were intraperitoneally administered for 4 weeks, respectively. Renal function and foot process proteins were analysed to evaluate the effects of apelin on kk-Ay mice and podocytes. Apelin increased albuminuria and decreased podocyte foot process proteins expression in kk-Ay mice, which is consistent with the results that apelin receptor (APLNR) levels increased in glomeruli of patients or mice with DN. In cultured podocytes, high glucose increased APLNR expression and apelin administration was associated with increased permeability and decreased foot process proteins levels. All these dysfunctions were associated with decreased 26S proteasome activities and increased polyubiquitinated proteins in both kk-Ay mice and cultured podocytes, as demonstrated by 26S proteasome activation with cyclic adenosine monophosphate (cAMP) or oleuropein. These effects seemed to be related to endoplasmic reticulum (ER) stress, as apelin increased C/EBP homologous protein (CHOP) and peiFα levels while cAMP or oleuropein reduced it in high glucose and apelin treated podocytes. These results suggest that apelin induces podocyte dysfunction in DN through ER stress which was induced by decreased proteasome activities in podocytes.

Indexed as

AlbuminsAnimalsApelin ReceptorsBasement MembraneCell Membrane PermeabilityCreatinineCyclic AMPDiabetes Mellitus, Type 2Diabetic NephropathiesEndoplasmic Reticulum StressFemaleGlucoseHumansIntercellular Signaling Peptides and ProteinsIridoid GlucosidesIridoidsAlbuminsapelin-13, Ala(13)-Apelin ReceptorsAplnr protein, mouseCreatinineCyclic AMPGlucoseIntercellular Signaling Peptides and ProteinsIridoid GlucosidesIridoidsoleuropeinProteasome Endopeptidase ComplexProteasome InhibitorsReceptors, G-Protein-CoupledapelinAPLNRdiabetic nephropathyER stresspodocyteproteasome

Identifiers

PMID26103809
PMCPMC4568931
OpenAlexW2113491624

What OpenQuestion holds

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LicenceCC BY
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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.