Redox regulation of sarcoplasmic reticulum calcium cycling in the heart

The coordinated release and reuptake of calcium into the sarcoplasmic reticulum (SR) is critical to maintain an adequate heart function. Reactive oxygen species (ROS) and reactive nitrogen species (RNS), generated in the heart under normal basal condition, modulate the function of different proteins...

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Detalles Bibliográficos
Autores principales: Donoso, Paulina, Sánchez, Gina
Formato: Articulo
Lenguaje:Inglés
Publicado: 2013
Materias:
Acceso en línea:http://sedici.unlp.edu.ar/handle/10915/131287
https://pmr.safisiol.org.ar/uploadsarchivos/redox_regulation_of_sr_calcium_cycling_in_the_heart_final_j1.pdf
Aporte de:
id I19-R120-10915-131287
record_format dspace
institution Universidad Nacional de La Plata
institution_str I-19
repository_str R-120
collection SEDICI (UNLP)
language Inglés
topic Ciencias Médicas
calcium cycling
sarcoplasmic reticulum
reactive oxygen species
reactive nitrogen species
spellingShingle Ciencias Médicas
calcium cycling
sarcoplasmic reticulum
reactive oxygen species
reactive nitrogen species
Donoso, Paulina
Sánchez, Gina
Redox regulation of sarcoplasmic reticulum calcium cycling in the heart
topic_facet Ciencias Médicas
calcium cycling
sarcoplasmic reticulum
reactive oxygen species
reactive nitrogen species
description The coordinated release and reuptake of calcium into the sarcoplasmic reticulum (SR) is critical to maintain an adequate heart function. Reactive oxygen species (ROS) and reactive nitrogen species (RNS), generated in the heart under normal basal condition, modulate the function of different proteins via the reversible oxidation of critical cysteine residues. Excess ROS/RNS generation has been shown to impair heart function, but extensive evidence indicates that the controlled production of these molecules increases cardiac contractility by targeting SR calcium proteins. Ryanodine receptors (RyR2) are endogenously S-nitrosylated and S-glutathionylated and both redox modifications increase the activity of these channels in vitro. Moreover, exercise or rapid pacing increases the RyR2 S-glutathionylation, a modification that depends on the activation of NADPH oxidase (NOX2). In isolated cardiomyocytes, this enzyme is rapidly activated by stretch, generating an immediate burst of ROS which increases calcium release by RyR2. Nitroxyl, a particular ROS/RNS, increases cardiac inotropy in vivo, by targeting critical thiols in RyR2, the SR Ca2+-ATPase and phospholamban, allowing the simultaneous increase in calcium release and reuptake, required to produce a sustained increase in the calcium transient. In this minireview we present some of the recent work on the redox regulation of SR calcium cycling proteins.
format Articulo
Articulo
author Donoso, Paulina
Sánchez, Gina
author_facet Donoso, Paulina
Sánchez, Gina
author_sort Donoso, Paulina
title Redox regulation of sarcoplasmic reticulum calcium cycling in the heart
title_short Redox regulation of sarcoplasmic reticulum calcium cycling in the heart
title_full Redox regulation of sarcoplasmic reticulum calcium cycling in the heart
title_fullStr Redox regulation of sarcoplasmic reticulum calcium cycling in the heart
title_full_unstemmed Redox regulation of sarcoplasmic reticulum calcium cycling in the heart
title_sort redox regulation of sarcoplasmic reticulum calcium cycling in the heart
publishDate 2013
url http://sedici.unlp.edu.ar/handle/10915/131287
https://pmr.safisiol.org.ar/uploadsarchivos/redox_regulation_of_sr_calcium_cycling_in_the_heart_final_j1.pdf
work_keys_str_mv AT donosopaulina redoxregulationofsarcoplasmicreticulumcalciumcyclingintheheart
AT sanchezgina redoxregulationofsarcoplasmicreticulumcalciumcyclingintheheart
bdutipo_str Repositorios
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