Evidence map›Paper›PMID 21420413›Full record

ArticleJournal of molecular and cellular cardiology2011

Nogo-A knockdown inhibits hypoxia/reoxygenation-induced activation of mitochondrial-dependent apoptosis in cardiomyocytes.

J P Sarkey, M Chu, M McShane, E Bovo, Y Ait Mou, A V Zima, P P de Tombe, G L Kartje, J L Martin

Abstract read
In one paragraph

Article in Journal of molecular and cellular cardiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
1.5field-weighted citation impact, top 19% 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

30 citing papers in PubMed, 45 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 2 institutions in 1 country.

J P SarkeyDepartment of Cell and Molecular Physiology, Loyola University Medical Center, Maywood, IL, USA. jsarkey@lumc.edu
M Chu
M McShane
E Bovo
Y Ait Mou
A V Zima
P P de Tombe
G L Kartje
J L Martin
Loyola University Medical Center · USEdward Hines, Jr. VA Hospital · US

Funding

Sarcomeric Modifications and Progressive Cardiac MaladaptationP01HL062426 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI AI, XUN · 2000 to 2020
$42.4M
TRAINING IN CELLULAR SIGNALLING IN THE CARDIOVASCULAR SYT32HL007692 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI SOLARO, R JOHN · 1990 to 2014
$8.5M
Neuron Plasticity and Recovery of Function After StrokeR01NS040960 · NINDS · LOYOLA UNIVERSITY CHICAGO · PI KARTJE, GWENDOLYN LOUISE · 2001 to 2010
$2.2M
Neuronal Plasticity and Recovery of Function After StrokeR56NS040960 · NINDS · LOYOLA UNIVERSITY CHICAGO · PI KARTJE, GWENDOLYN LOUISE · 2011 to 2011
$312k
Immunotherapy to Improve Functional Outcomes after Chronic Stoke in the AgedI01RX000828 · VA · EDWARD HINES JR VA HOSPITAL · PI KARTJE, GWENDOLYN LOUISE · 2012 to 2015
–
NHLBI NIH HHS HL62426NHLBI NIH HHS P01 HL062426NHLBI NIH HHS T32 HL007692NINDS NIH HHS 1R01NS40960NINDS NIH HHS R01 NS040960NINDS NIH HHS R56 NS040960PHS HHS PAF 2009-03479RRD VA I01 RX000828
6 · The paper itself

Abstract

Programmed cell death of cardiomyocytes following myocardial ischemia increases biomechanical stress on the remaining myocardium, leading to myocardial dysfunction that may result in congestive heart failure or sudden death. Nogo-A is well characterized as a potent inhibitor of axonal regeneration and plasticity in the central nervous system, however, the role of Nogo-A in non-nervous tissues is essentially unknown. In this study, Nogo-A expression was shown to be significantly increased in cardiac tissue from patients with dilated cardiomyopathy and from patients who have experienced an ischemic event. Nogo-A expression was clearly associated with cardiomyocytes in culture and was localized predominantly in the endoplasmic reticulum. In agreement with the findings from human tissue, Nogo-A expression was significantly increased in cultured neonatal rat cardiomyocytes subjected to hypoxia/reoxygenation. Knockdown of Nogo-A in cardiomyocytes markedly attenuated hypoxia/reoxygenation-induced apoptosis, as indicated by the significant reduction of DNA fragmentation, phosphatidylserine translocation, and caspase-3 cleavage, by a mechanism involving the preservation of mitochondrial membrane potential, the inhibition of ROS accumulation, and the improvement of intracellular calcium regulation. Together, these data demonstrate that knockdown of Nogo-A may serve as a novel therapeutic strategy to prevent the loss of cardiomyocytes following ischemic/hypoxic injury.

Indexed as

ApoptosisAnimalsCalciumCardiomyopathy, DilatedCaspase 3Cell HypoxiaCytochromes cDisease Models, AnimalDNA FragmentationEndoplasmic ReticulumGene Knockdown TechniquesHumansMembrane Potential, MitochondrialMitochondriaMyelin ProteinsMyocardial IschemiaCalciumCaspase 3Cytochromes cMyelin ProteinsNogo ProteinsPhosphatidylserinesReactive Oxygen SpeciesRTN4 protein, humanRtn4 protein, rat

Identifiers

PMID21420413
PMCPMC3091973
OpenAlexW2051898065

What OpenQuestion holds

Textmetadata
LicenceTDM
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.