Mitochondrial Oxidative Metabolism in Heart and Muscle

A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Health Outcomes of Antioxidants and Oxidative Stress".

Deadline for manuscript submissions: closed (31 July 2023) | Viewed by 1284

Special Issue Editor


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Guest Editor
Faculté de Pharmacie, UMR-S 1180, INSERM, Université Paris-Saclay, 17 Avenue des Sciences, 91400 Orsay, France
Interests: heart; cardiovascular diseases; mitochondria; mitochondrial oxidative metabolism; muscle

Special Issue Information

Dear Colleagues,

Beyond their well-known role in ATP production, mitochondria take part in many cellular processes, such as apoptosis, ion homeostasis, thermogenesis, and production of radical oxygen species (ROS). In cardiac muscle cells and skeletal muscle slow twitch fibers, mitochondria are the main energy producers and occupy a large volume of intracellular medium. Consequently, these myocytes are particularly exposed to mitochondrial ROS, which are inevitably produced when the mitochondrial electron transfer chain is working. While low production of ROS is an essential intracellular signal and participates in cellular homeostasis in cells with an appropriate antioxidant defense system, dysregulation of ROS production and/or degradation leads to oxidative stress, which can be a key element in the pathophysiology of cardiac and muscular diseases. This Special Issue focuses on recent research advances made to better understand mitochondrial oxidative metabolism in heart and skeletal muscle in physiology and pathophysiology and how this could be impacted by potential antioxidant compounds. We warmly welcome the submission of original papers and reviews addressing these topics.

Dr. Jérôme Piquereau
Guest Editor

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Keywords

  • mitochondrion
  • oxidative stress
  • heart
  • skeletal muscle
  • cardiac disease
  • myopathy

Published Papers (1 paper)

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Research

25 pages, 5686 KiB  
Article
Abscisic Acid and Its Receptors LANCL1 and LANCL2 Control Cardiomyocyte Mitochondrial Function, Expression of Contractile, Cytoskeletal and Ion Channel Proteins and Cell Proliferation via ERRα
by Sonia Spinelli, Lucrezia Guida, Mario Passalacqua, Mirko Magnone, Vanessa Cossu, Gianmario Sambuceti, Cecilia Marini, Laura Sturla and Elena Zocchi
Antioxidants 2023, 12(9), 1692; https://doi.org/10.3390/antiox12091692 - 30 Aug 2023
Cited by 2 | Viewed by 925
Abstract
The cross-kingdom stress hormone abscisic acid (ABA) and its mammalian receptors LANCL1 and LANCL2 regulate the response of cardiomyocytes to hypoxia by activating NO generation. The overexpression of LANCL1/2 increases transcription, phosphorylation and the activity of eNOS and improves cell vitality after hypoxia/reoxygenation [...] Read more.
The cross-kingdom stress hormone abscisic acid (ABA) and its mammalian receptors LANCL1 and LANCL2 regulate the response of cardiomyocytes to hypoxia by activating NO generation. The overexpression of LANCL1/2 increases transcription, phosphorylation and the activity of eNOS and improves cell vitality after hypoxia/reoxygenation via the AMPK/PGC-1α axis. Here, we investigated whether the ABA/LANCL system also affects the mitochondrial oxidative metabolism and structural proteins. Mitochondrial function, cell cycle and the expression of cytoskeletal, contractile and ion channel proteins were studied in H9c2 rat cardiomyoblasts overexpressing or silenced by LANCL1 and LANCL2, with or without ABA. Overexpression of LANCL1/2 significantly increased, while silencing conversely reduced the mitochondrial number, OXPHOS complex I, proton gradient, glucose and palmitate-dependent respiration, transcription of uncoupling proteins, expression of proteins involved in cytoskeletal, contractile and electrical functions. These effects, and LANCL1/2-dependent NO generation, are mediated by transcription factor ERRα, upstream of the AMPK/PGC1-α axis and transcriptionally controlled by the LANCL1/2–ABA system. The ABA-LANCL1/2 hormone-receptor system controls fundamental aspects of cardiomyocyte physiology via an ERRα/AMPK/PGC-1α signaling axis and ABA-mediated targeting of this axis could improve cardiac function and resilience to hypoxic and dysmetabolic conditions. Full article
(This article belongs to the Special Issue Mitochondrial Oxidative Metabolism in Heart and Muscle)
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