Evidence map›Paper›PMID 30005635›Full record

ArticleBMC nephrology2018

Angiotensin II-induced podocyte apoptosis is mediated by endoplasmic reticulum stress/PKC-δ/p38 MAPK pathway activation and trough increased Na

Vanessa Gerolde Cardoso, Guilherme Lopes Gonçalves, Juliana Martins Costa-Pessoa, Karina Thieme, Bruna Bezerra Lins, Fernando Augusto Malavazzi Casare, Mariana Charleaux de Ponte, Niels Olsen Saraiva Camara, Maria Oliveira-Souza

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

Article in BMC nephrology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

37 citing papers in PubMed, 57 citations in OpenAlex.

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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

9 authors at 1 institution in 1 country.

Vanessa Gerolde CardosoLaboratory of Renal Physiology, Department of Physiology and Biophysics, Institute of Biomedical Sciences, University of Sao Paulo, Sao Paulo, SP, 05508-900, Brazil.
Guilherme Lopes GonçalvesLaboratory of Renal Physiology, Department of Physiology and Biophysics, Institute of Biomedical Sciences, University of Sao Paulo, Sao Paulo, SP, 05508-900, Brazil.
Juliana Martins Costa-PessoaLaboratory of Renal Physiology, Department of Physiology and Biophysics, Institute of Biomedical Sciences, University of Sao Paulo, Sao Paulo, SP, 05508-900, Brazil.
Karina ThiemeLaboratory of Carbohydrates and Radioimmunoassays (LIM-18), Medical School, University of Sao Paulo, Sao Paulo, Brazil.
Bruna Bezerra LinsLaboratory of Renal Physiology, Department of Physiology and Biophysics, Institute of Biomedical Sciences, University of Sao Paulo, Sao Paulo, SP, 05508-900, Brazil.
Fernando Augusto Malavazzi CasareLaboratory of Renal Physiology, Department of Physiology and Biophysics, Institute of Biomedical Sciences, University of Sao Paulo, Sao Paulo, SP, 05508-900, Brazil.
Mariana Charleaux de PonteLaboratory of Renal Physiology, Department of Physiology and Biophysics, Institute of Biomedical Sciences, University of Sao Paulo, Sao Paulo, SP, 05508-900, Brazil.
Niels Olsen Saraiva CamaraLaboratory for Transplantation Immunobiology, Department of Immunology, Institute of Biomedical Sciences, University of Sao Paulo, Sao Paulo, Brazil.
Maria Oliveira-SouzaLaboratory of Renal Physiology, Department of Physiology and Biophysics, Institute of Biomedical Sciences, University of Sao Paulo, Sao Paulo, SP, 05508-900, Brazil. souza@icb.usp.br.
Universidade de São Paulo · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAngiotensin II (Ang II) contributes to the progression of renal diseases associated with proteinuria and glomerulosclerosis mainly by inducing podocyte apoptosis. In the present study, we investigated whether the chronic effects of Ang II via AT1 receptor (AT1R) would result in endoplasmic reticulum (ER) stress/PKC-delta/p38 MAPK stimulation, and consequently podocyte apoptosis.

methodsWistar rats were treated with Ang II (200 ng·kg

resultsCompared with controls, Ang II via AT1R increased chaperone GRP 78/Bip protein expression in rat glomeruli (p < 0.001) as well as in podocyte culture (p < 0.01); increased phosphorylated eIf2-α (p < 0.05), PKC-delta (p < 0.01) and p38 MAPK (p < 0.001) protein expression. Furthermore, Ang II induced p38 MAPK-mediated late apoptosis and increased the Bax/Bcl-2 ratio (p < 0.001). Simultaneously, Ang II via AT1R induced p38 MAPK-NHE1-mediated increase of pHi recovery rate after acid loading.

conclusionTogether, our results indicate that Ang II-induced podocyte apoptosis is associated with AT1R/ER stress/PKC-delta/p38 MAPK axis and enhanced NHE1-mediated pHi recovery rate.

Indexed as

Angiotensin IIAnimalsApoptosisCell Line, TransformedEndoplasmic Reticulum StressEnzyme ActivationMicep38 Mitogen-Activated Protein KinasesPodocytesProtein IsoformsProtein Kinase C-deltaRandom AllocationRatsRats, WistarSodium-Hydrogen Exchanger 1Angiotensin IIp38 Mitogen-Activated Protein KinasesProtein IsoformsProtein Kinase C-deltaSodium-Hydrogen Exchanger 1Angiotensin IIApoptosisNHE1p38 MAPKPKC-deltaPodocytes

Identifiers

PMID30005635
PMCPMC6043975
OpenAlexW2883496301

What OpenQuestion holds

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Registered trials

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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.