Evidence map›Paper›PMID 29295576›Full record

ArticleInternational journal of molecular sciences2017

Intracellular Renin Inhibits Mitochondrial Permeability Transition Pore via Activated Mitochondrial Extracellular Signal-Regulated Kinase (ERK) 1/2 during Ischemia in Diabetic Hearts.

Terumori Satoh, Masao Saotome, Hideki Katoh, Daishi Nonaka, Prottoy Hasan, Hideharu Hayashi, Yuichiro Maekawa

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.5field-weighted citation impact, top 28% 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

2 citing papers in PubMed, 5 citations in OpenAlex.

  1. Article
  2. Hydrogen sulfide inhibits CaAmerican journal of physiology. Endocrinology and metabolism · 2019
    Article
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.

Terumori SatohInternal Medicine III, Hamamatsu University School of Medicine, Hamamatsu 431-3192, Japan. terumori@hama-med.ac.jp.
Masao SaotomeInternal Medicine III, Hamamatsu University School of Medicine, Hamamatsu 431-3192, Japan. msaotome@hama-med.ac.jp.
Hideki KatohInternal Medicine III, Hamamatsu University School of Medicine, Hamamatsu 431-3192, Japan. hkatoh56@gmail.com.
Daishi NonakaInternal Medicine III, Hamamatsu University School of Medicine, Hamamatsu 431-3192, Japan. daishinonaka@gmail.com.
Prottoy HasanInternal Medicine III, Hamamatsu University School of Medicine, Hamamatsu 431-3192, Japan. dr.prottoyhasan@gmail.com.ORCID 0000-0001-9968-3400
Hideharu HayashiInternal Medicine III, Hamamatsu University School of Medicine, Hamamatsu 431-3192, Japan. hideharuhayashi@gmail.com.
Yuichiro MaekawaInternal Medicine III, Hamamatsu University School of Medicine, Hamamatsu 431-3192, Japan. ymaekawa@hama-med.ac.jp.
Hamamatsu University School of Medicine · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although beneficial effects of non-secreting intracellular renin (ns-renin) against ischemia have been reported, the precise mechanism remains unclear. In this study, we investigated the roles of ns-renin and mitochondrial extracellular signal-related kinase (ERK) 1/2 on mitochondrial permeability transition pore (mPTP) opening during ischemia in diabetes mellitus (DM) hearts. When isolated hearts from Wistar rats (non-DM hearts) and Goto-Kakizaki rats (DM hearts) were subjected to ischemia for 70 min by left anterior descending coronary artery ligation, DM hearts exhibited higher left ventricular (LV) developed pressure and lower LV end-diastolic pressure than non-DM hearts, suggesting ischemic resistance. In addition, DM hearts showed increased intracellular renin (int-renin, including secreting and non-secreting renin) in the ischemic area, and a direct renin inhibitor (DRI; aliskiren) attenuated ischemic resistance in DM hearts. ERK1/2 was significantly phosphorylated after ischemia in both whole cell and mitochondrial fractions in DM hearts. In isolated mitochondria from DM hearts, rat recombinant renin (r-renin) significantly phosphorylated mitochondrial ERK1/2, and hyperpolarized mitochondrial membrane potential (ΔΨ

Indexed as

AnimalsAtractylosideButadienesDiabetes Mellitus, ExperimentalEnzyme ActivationExtracellular Signal-Regulated MAP KinasesMitochondriaMitochondria, HeartMitochondrial Membrane Transport ProteinsMitochondrial Permeability Transition PoreMyocardial IschemiaNitrilesRatsRecombinant ProteinsReninAtractylosideButadienesExtracellular Signal-Regulated MAP KinasesMitochondrial Membrane Transport ProteinsMitochondrial Permeability Transition PoreNitrilesRecombinant ProteinsReninU 0126diabetes mellitusintracellular reninischemiamitochondrial ERK1/2mitochondrial permeability transition pore

Identifiers

PMID29295576
PMCPMC5796005
OpenAlexW2780860164

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.