Direct modulation of RyR2 leading to a tricky Ca2+ balance the effects of TRIC-A on cardiac muscle

Autores
Gonano, Luis Alberto; Vila Petroff, Martin Gerarde
Año de publicación
2020
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
A central point in heart research is to understand the mechanisms behind Ca2+ handling and to find alternatives to correct defective Ca2+ cycling associated with heart failure and arrhythmias. In cardiac myocytes, entry of Ca2+ occurs through L-type Ca2+ channels and mediates the opening of RyR2 (ryanodine receptor 2) channels allowing systolic movement of Ca2+ from the sarcoplasmic reticulum (SR) to the cytosol. In addition, SR Ca2+ release occurs randomly due to RyR2 opening in response to a combination of factors that favor (luminal and cytosolic Ca2+, ATP, posttranslational modifications; gain-of-function mutations or drugs) or preclude it (Mg2+, FKBPs, loss-of-function mutations or drugs). Due to its dependence on luminal SR Ca2+, the concept of SOICR (store overload-induced SR Ca2+ release) has emerged, and the capability of these events to generate delayed afterdepolarizations and arrhythmias is widely accepted. Thus, understanding the mechanisms that regulate SR Ca2+ release and its capacity to promote SOICR is of critical importance.
Fil: Gonano, Luis Alberto. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - La Plata. Centro de Investigaciones Cardiovasculares "Dr. Horacio Eugenio Cingolani". Universidad Nacional de La Plata. Facultad de Ciencias Médicas. Centro de Investigaciones Cardiovasculares "Dr. Horacio Eugenio Cingolani"; Argentina
Fil: Vila Petroff, Martin Gerarde. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - La Plata. Centro de Investigaciones Cardiovasculares "Dr. Horacio Eugenio Cingolani". Universidad Nacional de La Plata. Facultad de Ciencias Médicas. Centro de Investigaciones Cardiovasculares "Dr. Horacio Eugenio Cingolani"; Argentina
Materia
ANIMALS
EDITORIALS
HEART FAILURE
RYANODINE RECEPTOR CALCIUM RELEASE CHANNEL
SYSTOLE
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/142950
Acceder
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network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling Direct modulation of RyR2 leading to a tricky Ca2+ balance the effects of TRIC-A on cardiac muscleGonano, Luis AlbertoVila Petroff, Martin GerardeANIMALSEDITORIALSHEART FAILURERYANODINE RECEPTOR CALCIUM RELEASE CHANNELSYSTOLEhttps://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3A central point in heart research is to understand the mechanisms behind Ca2+ handling and to find alternatives to correct defective Ca2+ cycling associated with heart failure and arrhythmias. In cardiac myocytes, entry of Ca2+ occurs through L-type Ca2+ channels and mediates the opening of RyR2 (ryanodine receptor 2) channels allowing systolic movement of Ca2+ from the sarcoplasmic reticulum (SR) to the cytosol. In addition, SR Ca2+ release occurs randomly due to RyR2 opening in response to a combination of factors that favor (luminal and cytosolic Ca2+, ATP, posttranslational modifications; gain-of-function mutations or drugs) or preclude it (Mg2+, FKBPs, loss-of-function mutations or drugs). Due to its dependence on luminal SR Ca2+, the concept of SOICR (store overload-induced SR Ca2+ release) has emerged, and the capability of these events to generate delayed afterdepolarizations and arrhythmias is widely accepted. Thus, understanding the mechanisms that regulate SR Ca2+ release and its capacity to promote SOICR is of critical importance.Fil: Gonano, Luis Alberto. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - La Plata. Centro de Investigaciones Cardiovasculares "Dr. Horacio Eugenio Cingolani". Universidad Nacional de La Plata. Facultad de Ciencias Médicas. Centro de Investigaciones Cardiovasculares "Dr. Horacio Eugenio Cingolani"; ArgentinaFil: Vila Petroff, Martin Gerarde. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - La Plata. Centro de Investigaciones Cardiovasculares "Dr. Horacio Eugenio Cingolani". Universidad Nacional de La Plata. Facultad de Ciencias Médicas. Centro de Investigaciones Cardiovasculares "Dr. Horacio Eugenio Cingolani"; ArgentinaLippincott Williams2020-02-14info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/142950Gonano, Luis Alberto; Vila Petroff, Martin Gerarde; Direct modulation of RyR2 leading to a tricky Ca2+ balance the effects of TRIC-A on cardiac muscle; Lippincott Williams; Circulation Research; 126; 4; 14-2-2020; 436-4380009-73301524-4571CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/https://www.ahajournals.org/doi/10.1161/CIRCRESAHA.120.316532info:eu-repo/semantics/altIdentifier/doi/10.1161/CIRCRESAHA.120.316532info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-29T09:51:25Zoai:ri.conicet.gov.ar:11336/142950instacron:CONICETInstitucionalhttp://ri.conicet.gov.ar/Organismo científico-tecnológicoNo correspondehttp://ri.conicet.gov.ar/oai/requestdasensio@conicet.gov.ar; lcarlino@conicet.gov.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:34982025-09-29 09:51:25.506CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Direct modulation of RyR2 leading to a tricky Ca2+ balance the effects of TRIC-A on cardiac muscle
title Direct modulation of RyR2 leading to a tricky Ca2+ balance the effects of TRIC-A on cardiac muscle
spellingShingle Direct modulation of RyR2 leading to a tricky Ca2+ balance the effects of TRIC-A on cardiac muscle
Gonano, Luis Alberto
ANIMALS
EDITORIALS
HEART FAILURE
RYANODINE RECEPTOR CALCIUM RELEASE CHANNEL
SYSTOLE
title_short Direct modulation of RyR2 leading to a tricky Ca2+ balance the effects of TRIC-A on cardiac muscle
title_full Direct modulation of RyR2 leading to a tricky Ca2+ balance the effects of TRIC-A on cardiac muscle
title_fullStr Direct modulation of RyR2 leading to a tricky Ca2+ balance the effects of TRIC-A on cardiac muscle
title_full_unstemmed Direct modulation of RyR2 leading to a tricky Ca2+ balance the effects of TRIC-A on cardiac muscle
title_sort Direct modulation of RyR2 leading to a tricky Ca2+ balance the effects of TRIC-A on cardiac muscle
dc.creator.none.fl_str_mv Gonano, Luis Alberto
Vila Petroff, Martin Gerarde
author Gonano, Luis Alberto
author_facet Gonano, Luis Alberto
Vila Petroff, Martin Gerarde
author_role author
author2 Vila Petroff, Martin Gerarde
author2_role author
dc.subject.none.fl_str_mv ANIMALS
EDITORIALS
HEART FAILURE
RYANODINE RECEPTOR CALCIUM RELEASE CHANNEL
SYSTOLE
topic ANIMALS
EDITORIALS
HEART FAILURE
RYANODINE RECEPTOR CALCIUM RELEASE CHANNEL
SYSTOLE
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.1
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv A central point in heart research is to understand the mechanisms behind Ca2+ handling and to find alternatives to correct defective Ca2+ cycling associated with heart failure and arrhythmias. In cardiac myocytes, entry of Ca2+ occurs through L-type Ca2+ channels and mediates the opening of RyR2 (ryanodine receptor 2) channels allowing systolic movement of Ca2+ from the sarcoplasmic reticulum (SR) to the cytosol. In addition, SR Ca2+ release occurs randomly due to RyR2 opening in response to a combination of factors that favor (luminal and cytosolic Ca2+, ATP, posttranslational modifications; gain-of-function mutations or drugs) or preclude it (Mg2+, FKBPs, loss-of-function mutations or drugs). Due to its dependence on luminal SR Ca2+, the concept of SOICR (store overload-induced SR Ca2+ release) has emerged, and the capability of these events to generate delayed afterdepolarizations and arrhythmias is widely accepted. Thus, understanding the mechanisms that regulate SR Ca2+ release and its capacity to promote SOICR is of critical importance.
Fil: Gonano, Luis Alberto. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - La Plata. Centro de Investigaciones Cardiovasculares "Dr. Horacio Eugenio Cingolani". Universidad Nacional de La Plata. Facultad de Ciencias Médicas. Centro de Investigaciones Cardiovasculares "Dr. Horacio Eugenio Cingolani"; Argentina
Fil: Vila Petroff, Martin Gerarde. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - La Plata. Centro de Investigaciones Cardiovasculares "Dr. Horacio Eugenio Cingolani". Universidad Nacional de La Plata. Facultad de Ciencias Médicas. Centro de Investigaciones Cardiovasculares "Dr. Horacio Eugenio Cingolani"; Argentina
description A central point in heart research is to understand the mechanisms behind Ca2+ handling and to find alternatives to correct defective Ca2+ cycling associated with heart failure and arrhythmias. In cardiac myocytes, entry of Ca2+ occurs through L-type Ca2+ channels and mediates the opening of RyR2 (ryanodine receptor 2) channels allowing systolic movement of Ca2+ from the sarcoplasmic reticulum (SR) to the cytosol. In addition, SR Ca2+ release occurs randomly due to RyR2 opening in response to a combination of factors that favor (luminal and cytosolic Ca2+, ATP, posttranslational modifications; gain-of-function mutations or drugs) or preclude it (Mg2+, FKBPs, loss-of-function mutations or drugs). Due to its dependence on luminal SR Ca2+, the concept of SOICR (store overload-induced SR Ca2+ release) has emerged, and the capability of these events to generate delayed afterdepolarizations and arrhythmias is widely accepted. Thus, understanding the mechanisms that regulate SR Ca2+ release and its capacity to promote SOICR is of critical importance.
publishDate 2020
dc.date.none.fl_str_mv 2020-02-14
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
http://purl.org/coar/resource_type/c_6501
info:ar-repo/semantics/articulo
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv http://hdl.handle.net/11336/142950
Gonano, Luis Alberto; Vila Petroff, Martin Gerarde; Direct modulation of RyR2 leading to a tricky Ca2+ balance the effects of TRIC-A on cardiac muscle; Lippincott Williams; Circulation Research; 126; 4; 14-2-2020; 436-438
0009-7330
1524-4571
CONICET Digital
CONICET
url http://hdl.handle.net/11336/142950
identifier_str_mv Gonano, Luis Alberto; Vila Petroff, Martin Gerarde; Direct modulation of RyR2 leading to a tricky Ca2+ balance the effects of TRIC-A on cardiac muscle; Lippincott Williams; Circulation Research; 126; 4; 14-2-2020; 436-438
0009-7330
1524-4571
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/url/https://www.ahajournals.org/doi/10.1161/CIRCRESAHA.120.316532
info:eu-repo/semantics/altIdentifier/doi/10.1161/CIRCRESAHA.120.316532
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.format.none.fl_str_mv application/pdf
application/pdf
dc.publisher.none.fl_str_mv Lippincott Williams
publisher.none.fl_str_mv Lippincott Williams
dc.source.none.fl_str_mv reponame:CONICET Digital (CONICET)
instname:Consejo Nacional de Investigaciones Científicas y Técnicas
reponame_str CONICET Digital (CONICET)
collection CONICET Digital (CONICET)
instname_str Consejo Nacional de Investigaciones Científicas y Técnicas
repository.name.fl_str_mv CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicas
repository.mail.fl_str_mv dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar
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score 13.070432

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