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Role of Mitochondrial ROS for Calcium Alternans in Atrial Myocytes. | LitMetric

Role of Mitochondrial ROS for Calcium Alternans in Atrial Myocytes.

Biomolecules

Department of Physiology and Biophysics, Rush University Medical Center, 1750 W. Harrison St., Chicago, IL 60612, USA.

Published: January 2024

AI Article Synopsis

  • Research on isolated rabbit atrial myocytes showed that reactive oxygen species (ROS) production increases during CaT alternans and manipulating ROS levels can either enhance or alleviate these alternations.
  • Maintaining mitochondrial antioxidant defenses is essential for preventing harmful CaT alternans, suggesting that targeting mitochondrial redox states could be a potential treatment strategy for AF-related arrhythmias.

Article Abstract

Atrial calcium transient (CaT) alternans is defined as beat-to-beat alternations in CaT amplitude and is causally linked to atrial fibrillation (AF). Mitochondria play a significant role in cardiac excitation-contraction coupling and Ca signaling through redox environment regulation. In isolated rabbit atrial myocytes, ROS production is enhanced during CaT alternans, measured by fluorescence microscopy. Exogenous ROS (tert-butyl hydroperoxide) enhanced CaT alternans, whereas ROS scavengers (dithiothreitol, MnTBAP, quercetin, tempol) alleviated CaT alternans. While the inhibition of cellular NADPH oxidases had no effect on CaT alternans, interference with mitochondrial ROS (ROS) production had profound effects: (1) the superoxide dismutase mimetic MitoTempo diminished CaT alternans and shifted the pacing threshold to higher frequencies; (2) the inhibition of cyt peroxidase by SS-31, and inhibitors of ROS production by complexes of the electron transport chain S1QEL1.1 and S3QEL2, decreased the severity of CaT alternans; however (3) the impairment of mitochondrial antioxidant defense by the inhibition of nicotinamide nucleotide transhydrogenase with NBD-Cl and thioredoxin reductase-2 with auranofin enhanced CaT alternans. Our results suggest that intact mitochondrial antioxidant defense provides crucial protection against pro-arrhythmic CaT alternans. Thus, modulating the mitochondrial redox state represents a potential therapeutic approach for alternans-associated arrhythmias, including AF.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10887423PMC
http://dx.doi.org/10.3390/biom14020144DOI Listing

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