Evidence map›Paper›PMID 25237819›Full record

ArticlePloS one2014

Erythropoietin protects cardiomyocytes from cell death during hypoxia/reperfusion injury through activation of survival signaling pathways.

Asiya A Parvin, Raj A Pranap, U Shalini, Ajay Devendran, John E Baker, Anuradha Dhanasekaran

Erratum issuedOpen access · goldAbstract read
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. An erratum has been issued. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

14 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Observational
  7. Article
  8. Article
  9. Review
  10. Regeneration in the nervous system with erythropoietin.Frontiers in bioscience (Landmark edition) · 2016
    Review
  11. Review
  12. Erythropoietin and diabetes mellitus.World journal of diabetes · 2015
    Review
  13. Review
  14. Review
4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

6 authors at 2 institutions in 2 countries.

Asiya A ParvinCentre for Biotechnology, Anna University, Chennai, Tamil Nadu, India.
Raj A PranapCentre for Biotechnology, Anna University, Chennai, Tamil Nadu, India.
U ShaliniCentre for Biotechnology, Anna University, Chennai, Tamil Nadu, India.
Ajay DevendranCentre for Biotechnology, Anna University, Chennai, Tamil Nadu, India.
John E BakerDepartment of Surgery, Division of Cardiothoracic Surgery, Medical College of Wisconsin, Milwaukee, Wisconsin, United States of America.
Anuradha DhanasekaranCentre for Biotechnology, Anna University, Chennai, Tamil Nadu, India.
Anna University, Chennai · INMedical College of Wisconsin · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hypoxia/Reoxygenation (H/R) cardiac injury is of great importance in understanding Myocardial Infarctions, which affect a major part of the working population causing debilitating side effects and often-premature mortality. H/R injury primarily consists of apoptotic and necrotic death of cardiomyocytes due to a compromise in the integrity of the mitochondrial membrane. Major factors associated in the deregulation of the membrane include fluctuating reactive oxygen species (ROS), deregulation of mitochondrial permeability transport pore (MPTP), uncontrolled calcium (Ca2+) fluxes, and abnormal caspase-3 activity. Erythropoietin (EPO) is strongly inferred to be cardioprotective and acts by inhibiting the above-mentioned processes. Surprisingly, the underlying mechanism of EPO's action and H/R injury is yet to be fully investigated and elucidated. This study examined whether EPO maintains Ca2+ homeostasis and the mitochondrial membrane potential (ΔΨm) in cardiomyocytes when subjected to H/R injury and further explored the underlying mechanisms involved. H9C2 cells were exposed to different concentrations of EPO post-H/R, and 20 U/ml EPO was found to significantly increase cell viability by inhibiting the intracellular production of ROS and caspase-3 activity. The protective effect of EPO was abolished when H/R-induced H9C2 cells were treated with Wortmannin, an inhibitor of Akt, suggesting the mechanism of action through the activation Akt, a major survival pathway.

Indexed as

AnimalsCaspase 3Cell HypoxiaCell LineErythropoietinMembrane Potential, MitochondrialProtective AgentsRatsReactive Oxygen SpeciesReperfusion InjurySignal TransductionCaspase 3ErythropoietinProtective AgentsReactive Oxygen Species

Identifiers

PMID25237819
PMCPMC4169563
OpenAlexW2040583051

What OpenQuestion holds

Textmetadata
LicenceCC0
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.