Mitochondrial and Sarcoplasmic Reticulum Interconnection in Cardiac Arrhythmia
Ca2+ plays a pivotal role in mitochondrial energy production, contraction, and apoptosis. Mitochondrial Ca2+-targeted fluorescent probes have demonstrated that mitochondria Ca2+ transients are synchronized with Ca2+ fluxes occurring in the sarcoplasmic reticulum (SR). The presence of specialized pro...
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Frontiers Media S.A.
2021-01-01
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Online Access: | https://www.frontiersin.org/articles/10.3389/fcell.2020.623381/full |
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author | Felipe Salazar-Ramírez Roberto Ramos-Mondragón Roberto Ramos-Mondragón Gerardo García-Rivas Gerardo García-Rivas Gerardo García-Rivas |
author_facet | Felipe Salazar-Ramírez Roberto Ramos-Mondragón Roberto Ramos-Mondragón Gerardo García-Rivas Gerardo García-Rivas Gerardo García-Rivas |
author_sort | Felipe Salazar-Ramírez |
collection | DOAJ |
description | Ca2+ plays a pivotal role in mitochondrial energy production, contraction, and apoptosis. Mitochondrial Ca2+-targeted fluorescent probes have demonstrated that mitochondria Ca2+ transients are synchronized with Ca2+ fluxes occurring in the sarcoplasmic reticulum (SR). The presence of specialized proteins tethering SR to mitochondria ensures the local Ca2+ flux between these organelles. Furthermore, communication between SR and mitochondria impacts their functionality in a bidirectional manner. Mitochondrial Ca2+ uptake through the mitochondrial Ca2+ uniplex is essential for ATP production and controlled reactive oxygen species levels for proper cellular signaling. Conversely, mitochondrial ATP ensures the proper functioning of SR Ca2+-handling proteins, which ensures that mitochondria receive an adequate supply of Ca2+. Recent evidence suggests that altered SR Ca2+ proteins, such as ryanodine receptors and the sarco/endoplasmic reticulum Ca2+ ATPase pump, play an important role in maintaining proper cardiac membrane excitability, which may be initiated and potentiated when mitochondria are dysfunctional. This recognized mitochondrial role offers the opportunity to develop new therapeutic approaches aimed at preventing cardiac arrhythmias in cardiac disease. |
first_indexed | 2024-12-18T00:10:02Z |
format | Article |
id | doaj.art-c9a1a5dd5444496a81112777499b6569 |
institution | Directory Open Access Journal |
issn | 2296-634X |
language | English |
last_indexed | 2024-12-18T00:10:02Z |
publishDate | 2021-01-01 |
publisher | Frontiers Media S.A. |
record_format | Article |
series | Frontiers in Cell and Developmental Biology |
spelling | doaj.art-c9a1a5dd5444496a81112777499b65692022-12-21T21:27:43ZengFrontiers Media S.A.Frontiers in Cell and Developmental Biology2296-634X2021-01-01810.3389/fcell.2020.623381623381Mitochondrial and Sarcoplasmic Reticulum Interconnection in Cardiac ArrhythmiaFelipe Salazar-Ramírez0Roberto Ramos-Mondragón1Roberto Ramos-Mondragón2Gerardo García-Rivas3Gerardo García-Rivas4Gerardo García-Rivas5Tecnologico de Monterrey, Escuela de Medicina y Ciencias de la Salud, Cátedra de Cardiología y Medicina Cardiovascular, Monterrey, MexicoDepartment of Pharmacology, University of Michigan Medical School, Ann Arbor, MI, United StatesDepartment of Internal Medicine, Division of Cardiovascular Medicine, University of Michigan Medical School, Ann Arbor, MI, United StatesTecnologico de Monterrey, Escuela de Medicina y Ciencias de la Salud, Cátedra de Cardiología y Medicina Cardiovascular, Monterrey, MexicoTecSalud, Centro de Investigación Biomédica, Hospital Zambrano-Hellion, San Pedro Garza García, MexicoTecSalud, Centro de Medicina Funcional, Hospital Zambrano-Hellion, San Pedro Garza García, MexicoCa2+ plays a pivotal role in mitochondrial energy production, contraction, and apoptosis. Mitochondrial Ca2+-targeted fluorescent probes have demonstrated that mitochondria Ca2+ transients are synchronized with Ca2+ fluxes occurring in the sarcoplasmic reticulum (SR). The presence of specialized proteins tethering SR to mitochondria ensures the local Ca2+ flux between these organelles. Furthermore, communication between SR and mitochondria impacts their functionality in a bidirectional manner. Mitochondrial Ca2+ uptake through the mitochondrial Ca2+ uniplex is essential for ATP production and controlled reactive oxygen species levels for proper cellular signaling. Conversely, mitochondrial ATP ensures the proper functioning of SR Ca2+-handling proteins, which ensures that mitochondria receive an adequate supply of Ca2+. Recent evidence suggests that altered SR Ca2+ proteins, such as ryanodine receptors and the sarco/endoplasmic reticulum Ca2+ ATPase pump, play an important role in maintaining proper cardiac membrane excitability, which may be initiated and potentiated when mitochondria are dysfunctional. This recognized mitochondrial role offers the opportunity to develop new therapeutic approaches aimed at preventing cardiac arrhythmias in cardiac disease.https://www.frontiersin.org/articles/10.3389/fcell.2020.623381/fullmitochondriasarcoplasmic reticulumarrhythmiacalciumheart failureischemia/reperfusion injury |
spellingShingle | Felipe Salazar-Ramírez Roberto Ramos-Mondragón Roberto Ramos-Mondragón Gerardo García-Rivas Gerardo García-Rivas Gerardo García-Rivas Mitochondrial and Sarcoplasmic Reticulum Interconnection in Cardiac Arrhythmia Frontiers in Cell and Developmental Biology mitochondria sarcoplasmic reticulum arrhythmia calcium heart failure ischemia/reperfusion injury |
title | Mitochondrial and Sarcoplasmic Reticulum Interconnection in Cardiac Arrhythmia |
title_full | Mitochondrial and Sarcoplasmic Reticulum Interconnection in Cardiac Arrhythmia |
title_fullStr | Mitochondrial and Sarcoplasmic Reticulum Interconnection in Cardiac Arrhythmia |
title_full_unstemmed | Mitochondrial and Sarcoplasmic Reticulum Interconnection in Cardiac Arrhythmia |
title_short | Mitochondrial and Sarcoplasmic Reticulum Interconnection in Cardiac Arrhythmia |
title_sort | mitochondrial and sarcoplasmic reticulum interconnection in cardiac arrhythmia |
topic | mitochondria sarcoplasmic reticulum arrhythmia calcium heart failure ischemia/reperfusion injury |
url | https://www.frontiersin.org/articles/10.3389/fcell.2020.623381/full |
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