ArticleBiophysical journal2013
Mitochondrial colocalization with Ca2+ release sites is crucial to cardiac metabolism.
Article in Biophysical journal, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 20 citations in OpenAlex.
- Review
- Excitation and mechanical contraction of a 3D cardiomyocyte model.Biophysical journal · 2025Article
- Reactive oxygen species, toxicity, oxidative stress, and antioxidants: chronic diseases and aging.Archives of toxicology · 2023Review
- The pulse light mode enhances the effect of photobiomodulation on B16F10 melanoma cells through autophagy pathway.Lasers in medical science · 2023Article
- Insights on the impact of mitochondrial organisation on bioenergetics in high-resolution computational models of cardiac cell architecture.PLoS computational biology · 2018Article
- Computational Model of Calcium Signaling in Cardiac Atrial Cells at the Submicron Scale.Frontiers in physiology · 2018Article
- ROS and ROS-Mediated Cellular Signaling.Oxidative medicine and cellular longevity · 2016Review
- Examination of the Effects of Heterogeneous Organization of RyR Clusters, Myofibrils and Mitochondria on Ca2+ Release Patterns in Cardiomyocytes.PLoS computational biology · 2015Article
- Distinct functional roles of cardiac mitochondrial subpopulations revealed by a 3D simulation model.Biophysical journal · 2015Article
- An integrated finite element simulation of cardiomyocyte function based on triphasic theory.Frontiers in physiology · 2015Article
- Defective sarcoplasmic reticulum-mitochondria calcium exchange in aged mouse myocardium.Cell death & disease · 2014Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In cardiomyocyte subcellular structures, colocalization of mitochondria with Ca2+ release sites is implicated in regulation of cardiac energetics by facilitating Ca2+ influx into mitochondria to modulate the tricarboxylic acid (TCA) cycle. However, current experimental techniques limit detailed examination of this regulatory mechanism. Earlier, we developed a three-dimensional (3D) finite-element cardiomyocyte model featuring a subcellular structure that integrates excitation-contraction coupling and energy metabolism. Here, using this model, we examined the influence of distance between mitochondria and Ca2+ release sites by comparing a normal (50-nm) distance model and a large (200-nm) distance model (LD). The influence of distance was minimal under a low pacing rate (0.25 Hz), but under a higher pacing rate (2 Hz), lower levels of mitochondrial Ca2+ and NADH, elevated phosphate, and suppressed force generation became apparent in the LD model. Such differences became greater when functional impairments (reduced TCA cycle activity, uncoupling effect, and failing excitation-contraction coupling) were additionally imposed. We concluded that juxtaposition of the mitochondria and the Ca2+ release sites is crucial for rapid signal transmission to maintain cardiac-energy balance. The idealized 3D model of cardiac excitation-contraction and metabolism is a powerful tool to study cardiac energetics.
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