Evidence map›Paper›PMID 21486840›Full record

ArticleThe Journal of physiology2011

Mitochondrial production of reactive oxygen species contributes to the β-adrenergic stimulation of mouse cardiomycytes.

Daniel C Andersson, Jérémy Fauconnier, Takashi Yamada, Alain Lacampagne, Shi-Jin Zhang, Abram Katz, Håkan Westerblad

Open access · greenAbstract read
In one paragraph

Article in The Journal of physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed
6.8field-weighted citation impact, top 3% 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

67 citing papers in PubMed, 134 citations in OpenAlex.

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  7. Mitochondrial connexin43 and mitochondrial KPflugers Archiv : European journal of physiology · 2023
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  12. Citrullination is linked to reduced CaActa physiologica (Oxford, England) · 2022
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7 more citing papers are in PubMed but not listed here.

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 4 institutions in 4 countries.

Daniel C AnderssonDepartment of Physiology and Pharmacology, Karolinska Institutet, 171 77 Stockholm, Sweden.
Jérémy Fauconnier
Takashi Yamada
Alain Lacampagne
Shi-Jin Zhang
Abram Katz
Håkan Westerblad
Karolinska Institutet · SEInserm · FRPhysiologie et Médecine Expérimentale du Coeur et des Muscles · FRRMIT University · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The sympathetic adrenergic system plays a central role in stress signalling and stress is often associated with increased production of reactive oxygen species (ROS). Furthermore, the sympathetic adrenergic system is intimately involved in the regulation of cardiomyocyte Ca2+ handling and contractility. In this study we hypothesize that endogenously produced ROS contribute to the inotropic mechanism of β-adrenergic stimulation in mouse cardiomyocytes. Cytoplasmic Ca2+ transients, cell shortening and ROS production were measured in freshly isolated cardiomyocytes using confocal microscopy and fluorescent indicators. As a marker of oxidative stress, malondialdehyde (MDA) modification of proteins was detected with Western blotting. Isoproterenol (ISO), a β-adrenergic agonist, increased mitochondrial ROS production in cardiomyocytes in a concentration- and cAMP–protein kinase A-dependent but Ca2+-independent manner. Hearts perfused with ISO showed a twofold increase in MDA protein adducts relative to control. ISO increased Ca2+ transient amplitude, contraction and L-type Ca2+ current densities (measured with whole-cell patch-clamp) in cardiomyocytes and these increases were diminished by application of the general antioxidant N-acetylcysteine (NAC) or the mitochondria-targeted antioxidant SS31. In conclusion, increased mitochondrial ROS production plays an integral role in the acute inotropic response of cardiomyocytes to β-adrenergic stimulation. On the other hand, chronically sustained adrenergic stress is associated with the development of heart failure and cardiac arrhythmias and prolonged increases in ROS may contribute to these defects.

Indexed as

AcetylcysteineAdrenergic beta-AgonistsAnimalsAntioxidantsCalcium SignalingIn Vitro TechniquesIsoproterenolMembrane Potential, MitochondrialMiceMice, Inbred C57BLMitochondria, HeartMyocardial ContractionMyocytes, CardiacPatch-Clamp TechniquesReactive Oxygen SpeciesReceptors, Adrenergic, betaAcetylcysteineAdrenergic beta-AgonistsAntioxidantsIsoproterenolReactive Oxygen SpeciesReceptors, Adrenergic, beta

Identifiers

PMID21486840
PMCPMC3099030
OpenAlexW1497333599

What OpenQuestion holds

Textmetadata
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.