Calcium and TFAM crosstalk in the mitochondrial life cycle in cardiomyocytes

Calcium (Ca2+) links the electrical signals of the heart to the mechanical action of contraction in a process referred to as the cardiac excitation-contraction (EC) coupling, a process that consumes a large amount of adenosine triphosphate (ATP). The majority of ATP is produced in the mitochondria v...

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Autores principales: Cardetti, Caitlyn, Tigano, Marco, Sheu, Shey-Shing
Formato: Articulo
Lenguaje:Inglés
Publicado: 2023
Materias:
Ciencias Médicas
Biología
mitochondria
calcium
TFAM
cardiomyocytes
heart
mitocondrias
calcio
cardiomiocitos
corazón
Acceso en línea:http://sedici.unlp.edu.ar/handle/10915/163606
Aporte de:
SEDICI (UNLP) de Universidad Nacional de La Plata
id I19-R120-10915-163606
record_format dspace
spelling I19-R120-10915-1636062024-03-11T17:34:55Z http://sedici.unlp.edu.ar/handle/10915/163606 Calcium and TFAM crosstalk in the mitochondrial life cycle in cardiomyocytes Cardetti, Caitlyn Tigano, Marco Sheu, Shey-Shing 2023-08 2024-03-08T17:13:43Z en Ciencias Médicas Biología mitochondria calcium TFAM cardiomyocytes heart mitocondrias calcio cardiomiocitos corazón Calcium (Ca2+) links the electrical signals of the heart to the mechanical action of contraction in a process referred to as the cardiac excitation-contraction (EC) coupling, a process that consumes a large amount of adenosine triphosphate (ATP). The majority of ATP is produced in the mitochondria via oxidative phosphorylation (OXPHOS), which is linked to Ca2+ flux. The OXPHOS system is regulated by both the nuclear and mitochondrial genome, with mitochondrial transcription factor A (TFAM) being a major regulator of the latter. This mini review focuses on summarizing the limited literature implicating crosstalk between Ca2+ and TFAM in the adult cardiomyocyte throughout the mitochondrial life cycle: mitochondrial dynamics, biogenesis, and mitophagy. The goal of this review is to highlight gaps and fuel further investigation of the proposed Ca2+-TFAM axis. This research area has high potential to propel the development of therapeutic strategies targeting cardiovascular diseases such as heart failure. El calcio (Ca2+) vincula las señales eléctricas del corazón con la acción mecánica de la contracción en un proceso denominado acoplamiento excitación-contracción (EC) cardíaco, un proceso que consume una gran cantidad de trifosfato de adenosina (ATP). La mayor parte del ATP se produce en las mitocondrias mediante fosforilación oxidativa (OXPHOS), que está ligada al flujo de Ca2+. El sistema OXPHOS está regulado tanto por el genoma nuclear como por el mitocondrial, siendo el factor de transcripción mitocondrial A (TFAM) un importante regulador de este último. Esta mini revisión se centra en resumir la literatura limitada que implica la interferencia entre Ca2+ y TFAM en el cardiomiocito adulto a lo largo del ciclo de vida mitocondrial: dinámica mitocondrial, biogénesis y mitofagia. El objetivo de esta revisión es resaltar las brechas e impulsar una mayor investigación del eje Ca2+-TFAM propuesto. Esta área de investigación tiene un gran potencial para impulsar el desarrollo de estrategias terapéuticas dirigidas a enfermedades cardiovasculares como la insuficiencia cardíaca. Sociedad Argentina de Fisiología Articulo Articulo http://creativecommons.org/licenses/by-nc-sa/4.0/ Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0) application/pdf 35-46
institution Universidad Nacional de La Plata
institution_str I-19
repository_str R-120
collection SEDICI (UNLP)
language Inglés
topic Ciencias Médicas
Biología
mitochondria
calcium
TFAM
cardiomyocytes
heart
mitocondrias
calcio
cardiomiocitos
corazón
spellingShingle Ciencias Médicas
Biología
mitochondria
calcium
TFAM
cardiomyocytes
heart
mitocondrias
calcio
cardiomiocitos
corazón
Cardetti, Caitlyn
Tigano, Marco
Sheu, Shey-Shing
Calcium and TFAM crosstalk in the mitochondrial life cycle in cardiomyocytes
topic_facet Ciencias Médicas
Biología
mitochondria
calcium
TFAM
cardiomyocytes
heart
mitocondrias
calcio
cardiomiocitos
corazón
description Calcium (Ca2+) links the electrical signals of the heart to the mechanical action of contraction in a process referred to as the cardiac excitation-contraction (EC) coupling, a process that consumes a large amount of adenosine triphosphate (ATP). The majority of ATP is produced in the mitochondria via oxidative phosphorylation (OXPHOS), which is linked to Ca2+ flux. The OXPHOS system is regulated by both the nuclear and mitochondrial genome, with mitochondrial transcription factor A (TFAM) being a major regulator of the latter. This mini review focuses on summarizing the limited literature implicating crosstalk between Ca2+ and TFAM in the adult cardiomyocyte throughout the mitochondrial life cycle: mitochondrial dynamics, biogenesis, and mitophagy. The goal of this review is to highlight gaps and fuel further investigation of the proposed Ca2+-TFAM axis. This research area has high potential to propel the development of therapeutic strategies targeting cardiovascular diseases such as heart failure.
format Articulo
Articulo
author Cardetti, Caitlyn
Tigano, Marco
Sheu, Shey-Shing
author_facet Cardetti, Caitlyn
Tigano, Marco
Sheu, Shey-Shing
author_sort Cardetti, Caitlyn
title Calcium and TFAM crosstalk in the mitochondrial life cycle in cardiomyocytes
title_short Calcium and TFAM crosstalk in the mitochondrial life cycle in cardiomyocytes
title_full Calcium and TFAM crosstalk in the mitochondrial life cycle in cardiomyocytes
title_fullStr Calcium and TFAM crosstalk in the mitochondrial life cycle in cardiomyocytes
title_full_unstemmed Calcium and TFAM crosstalk in the mitochondrial life cycle in cardiomyocytes
title_sort calcium and tfam crosstalk in the mitochondrial life cycle in cardiomyocytes
publishDate 2023
url http://sedici.unlp.edu.ar/handle/10915/163606
work_keys_str_mv AT cardetticaitlyn calciumandtfamcrosstalkinthemitochondriallifecycleincardiomyocytes
AT tiganomarco calciumandtfamcrosstalkinthemitochondriallifecycleincardiomyocytes
AT sheusheyshing calciumandtfamcrosstalkinthemitochondriallifecycleincardiomyocytes
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