Evidence map›Paper›PMID 23530756›Full record

ArticleBritish journal of pharmacology2013

Activation of mitochondrial function and Hb expression in non-haematopoietic cells by an EPO inducer ameliorates ischaemic diseases in mice.

Pei-Lun Hsu, Lin-Yea Horng, Kang-Yung Peng, Chia-Ling Wu, Hui-Ching Sung, Rong-Tsun Wu

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Article in British journal of pharmacology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.6field-weighted citation impact, top 33% 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

8 citing papers in PubMed, 9 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. CaM kinase II regulates cardiac hemoglobin expression through histone phosphorylation upon sympathetic activation.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  5. Review
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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

6 authors at 2 institutions in 1 country.

Pei-Lun HsuInstitute of Biopharmaceutical Sciences, National Yang-Ming University, Taipei, Taiwan.
Lin-Yea Horng
Kang-Yung Peng
Chia-Ling Wu
Hui-Ching Sung
Rong-Tsun Wu
National Yang Ming Chiao Tung University · TWNational Yang Ming Chiao Tung University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

background and purposeMany organs suffer from ischaemic injuries that reduce their ability to generate sufficient energy, which is required for functional maintenance and repair. Erythropoietin (EPO) ameliorates ischaemic injuries by pleiotropic effects. The aim of this study was to investigate the effect and mechanism of a small molecule EH-201, and found it as a potent EPO inducer and its effect in non-haematopoietic cells for therapeutic potential in ischemic disorders. EXPERIMENTAL APPROACH: Mice kidney slices, primary hepatocytes, primary cardiomyocytes and C2C12 myoblasts were treated with EH-201. The effects of this treatment on EPO, Hb expression and mitochondrial biogenesis were analysed. In vivo, doxorubicin-induced cardiomyopathic mice were treated with EH-201. The mice were subjected to an endurance test, electrocardiography and echocardiography, and a histological examination of the isolated hearts was performed. EH-201 was also administered to cisplatin-induced nephropathic mice. KEY

resultsIn non-haematopoietic cells, EH-201 was potent at inducing EPO. EH-201 also stimulated mitochondrial biogenesis and enhanced the expression of Hb by a mechanism dependent on EPO-mediated signalling. In mechanistic studies, using EPO and EPO receptor-neutralizing antibodies, we confirmed that EH-201 enhances EPO-EPOR autocrine activity. EH-201 robustly increased the endurance performance activity of healthy and cardiomyopathic mice during hypoxic stress, enhanced myocardial mitochondrial biogenesis and Hb expression, and also improved cardiac function. EH-201 ameliorated anaemia and renal dysfunction in nephropathic mice. CONCLUSIONS AND IMPLICATIONS: The enhancement and recovery of cellular functions through the stimulation of mitochondrial activity and Hb production in non-haematopoietic cells by an inducer of endogenous EPO has potential as a therapeutic strategy for ischaemic diseases.

Indexed as

AnimalsCardiovascular DiseasesCell LineCells, CulturedCisplatinDoxorubicinErythropoietinGlucosidesHEK293 CellsHemoglobinsHepatocytesHumansKidneyMaleMiceMice, Inbred C57BL2,3,5,4'-tetrahydroxystilbene 2-O-glucopyranosideCisplatinDoxorubicinErythropoietinGlucosidesHemoglobinsReceptors, ErythropoietinStilbenesanaemiacardiomyopathyendurance performanceerythropoietinhaemoglobininducerischaemic diseasemitochondrianon-haematopoietic cell

Identifiers

PMID23530756
PMCPMC3724104
OpenAlexW1593297041

What OpenQuestion holds

Textmetadata
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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.