Evidence map›Paper›PMID 24747517›Full record

ArticlePloS one2014

Ghrelin protects against renal damages induced by angiotensin-II via an antioxidative stress mechanism in mice.

Keiko Fujimura, Shu Wakino, Hitoshi Minakuchi, Kazuhiro Hasegawa, Koji Hosoya, Motoaki Komatsu, Yuka Kaneko, Keisuke Shinozuka, Naoki Washida, Takeshi Kanda and 3 more

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

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
2.4field-weighted citation impact, top 12% 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, 1 synthesis or guideline pooled it, 44 citations in OpenAlex.

  1. Potentiality of ghrelin as antioxidant and protective agent.Redox report : communications in free radical research · 2021
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  5. Renal Ghrelin-Family GPR39 Receptor and Urinary Concentrating Ability.Journal of the American Society of Nephrology : JASN · 2025
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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

13 authors at 1 institution in 1 country.

Keiko FujimuraDepartment of Internal Medicine, School of Medicine, Keio University, Tokyo, Japan.
Shu WakinoDepartment of Internal Medicine, School of Medicine, Keio University, Tokyo, Japan.
Hitoshi MinakuchiDepartment of Internal Medicine, School of Medicine, Keio University, Tokyo, Japan.
Kazuhiro HasegawaDepartment of Internal Medicine, School of Medicine, Keio University, Tokyo, Japan.
Koji HosoyaDepartment of Internal Medicine, School of Medicine, Keio University, Tokyo, Japan.
Motoaki KomatsuDepartment of Internal Medicine, School of Medicine, Keio University, Tokyo, Japan.
Yuka KanekoDepartment of Internal Medicine, School of Medicine, Keio University, Tokyo, Japan.
Keisuke ShinozukaDepartment of Internal Medicine, School of Medicine, Keio University, Tokyo, Japan.
Naoki WashidaDepartment of Internal Medicine, School of Medicine, Keio University, Tokyo, Japan.
Takeshi KandaDepartment of Internal Medicine, School of Medicine, Keio University, Tokyo, Japan.
Hirobumi TokuyamaDepartment of Internal Medicine, School of Medicine, Keio University, Tokyo, Japan.
Koichi HayashiDepartment of Internal Medicine, School of Medicine, Keio University, Tokyo, Japan.
Hiroshi ItohDepartment of Internal Medicine, School of Medicine, Keio University, Tokyo, Japan.
Keio University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We explored the renal protective effects by a gut peptide, Ghrelin. Daily peritoneal injection with Ghrelin ameliorated renal damages in continuously angiotensin II (AngII)-infused C57BL/6 mice as assessed by urinary excretion of protein and renal tubular markers. AngII-induced increase in reactive oxygen species (ROS) levels and senescent changes were attenuated by Ghrelin. Ghrelin also inhibited AngII-induced upregulations of transforming growth factor-β (TGF-β) and plasminogen activator inhibitor-1 (PAI-1), ameliorating renal fibrotic changes. These effects were accompanied by concomitant increase in mitochondria uncoupling protein, UCP2 as well as in a key regulator of mitochondria biosynthesis, PGC1α. In renal proximal cell line, HK-2 cells, Ghrelin reduced mitochondria membrane potential and mitochondria-derived ROS. The transfection of UCP2 siRNA abolished the decrease in mitochondria-derived ROS by Ghrelin. Ghrelin ameliorated AngII-induced renal tubular cell senescent changes and AngII-induced TGF-β and PAI-1 expressions. Finally, Ghrelin receptor, growth hormone secretagogue receptor (GHSR)-null mice exhibited an increase in tubular damages, renal ROS levels, renal senescent changes and fibrosis complicated with renal dysfunction. GHSR-null mice harbored elongated mitochondria in the proximal tubules. In conclusion, Ghrelin suppressed AngII-induced renal damages through its UCP2 dependent anti-oxidative stress effect and mitochondria maintenance. Ghrelin/GHSR pathway played an important role in the maintenance of ROS levels in the kidney.

Indexed as

Angiotensin IIAnimalsCell LineCellular SenescenceCytoprotectionFibrosisGene Expression RegulationGene Knockout TechniquesGhrelinHumansIon ChannelsKidneyKidney Tubules, ProximalMaleMiceMitochondriaAngiotensin IIGhrelinIon ChannelsMitochondrial ProteinsReactive Oxygen SpeciesReceptors, GhrelinUCP2 protein, humanUcp2 protein, mouseUncoupling Protein 2

Identifiers

PMID24747517
PMCPMC3991592
OpenAlexW1995743466

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.