Targeting the mitochondrial Ca2+ uniporter complex in cardiovascular disease

Cardiovascular diseases (CVDs), the leading cause of death worldwide, share in common mitochondrial dysfunction, in specific a dysregulation of Ca2+ uptake dynamics through the mitochondrial Ca2+ uniporter (MCU) complex. In particular, Ca2+ uptake regulates the mitochondrial ATP production, mitochon...

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Bibliographic Details
Published in:Acta Physiologica 2023-04, Vol.237 (4), p.e13946-n/a
Main Authors: Lozano, Omar, Marcos, Patricio, Salazar‐Ramirez, Felipe de Jesús, Lázaro‐Alfaro, Anay F., Sobrevia, Luis, García‐Rivas, Gerardo
Format: Article
Language:English
Subjects:
Calcium (mitochondrial)
Calcium influx
Calcium signalling
Cardiovascular diseases
Cell death
gene therapy
Mitochondria
mitochondrial Ca2+ uniporter
mitochondrial Ca2+ uptake
Oxidative stress
pharmacological therapy
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Summary:Cardiovascular diseases (CVDs), the leading cause of death worldwide, share in common mitochondrial dysfunction, in specific a dysregulation of Ca2+ uptake dynamics through the mitochondrial Ca2+ uniporter (MCU) complex. In particular, Ca2+ uptake regulates the mitochondrial ATP production, mitochondrial dynamics, oxidative stress, and cell death. Therefore, modulating the activity of the MCU complex to regulate Ca2+ uptake, has been suggested as a potential therapeutic approach for the treatment of CVDs. Here, the role and implications of the MCU complex in CVDs are presented, followed by a review of the evidence for MCU complex modulation, genetically and pharmacologically. While most approaches have aimed within the MCU complex for the modulation of the Ca2+ pore channel, the MCU subunit, its intra‐ and extra‐ mitochondrial implications, including Ca2+ dynamics, oxidative stress, post‐translational modifications, and its repercussions in the cardiac function, highlight that targeting the MCU complex has the translational potential for novel CVDs therapeutics.
ISSN:1748-1708
1748-1716
DOI:10.1111/apha.13946