ArticleBiochemistry2013
Effect of calcium on the oxidative phosphorylation cascade in skeletal muscle mitochondria.
Article in Biochemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 196 papers.
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Who cites it
196 citing papers in PubMed, 300 citations in OpenAlex.
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- Mitochondrial Dysfunction in Traumatic Brain Injury and Its Theranostic Implications.Biomolecules · 2026Review
- A paradoxical relationship between mitochondrial calcium regulation and retinal ganglion cell degeneration after axon damage.bioRxiv : the preprint server for biology · 2026Article
- Accumulated mtDNA mutations are linked to specific impairments in NADH-linked respiration.iScience · 2026Article
- Emerging roles of microRNAs and other non-coding transcriptome in muscular dystrophies.Inflammation and regeneration · 2026Review
- Neurometabolic substrate utilization governs oxidative phosphorylation conductance in cortex and hippocampus.Journal of neurophysiology · 2026Article
- Exercise-Induced Molecular Adaptations in Chronic Non-Communicable Diseases-Narrative Review.International journal of molecular sciences · 2025Review
- Rapid mitochondrial repolarization upon reperfusion after cardiac ischemia.Nature cardiovascular research · 2025Article
- Nonfat Milk Supplementation Mitigates Hepatic Lipid Accumulation and Improves Hepatic Lipid Metabolism in an Early Metabolic Dysfunction-Associated Steatotic Liver Disease C57BL/6N Mouse Model.The Journal of nutrition · 2025Article
- Mitochondrial respiratory function in human platelets: Influence of sample preparation, assay buffer, and instrumental platform.Physiological reports · 2025Article
- Ryanodine receptor stabilizer S-107 rescues slow-type rat soleus muscle function after 7-day hindlimb unloading.Pflugers Archiv : European journal of physiology · 2025Article
- Mitochondrial CaJournal of cellular physiology · 2025Review
- Mitochondrial diagnostics reveal diffuse impairments in skeletal muscle energetics in aging mice.Journal of applied physiology (Bethesda, Md. : 1985) · 2025Article
- Mitochondria-Associated Membrane Dysfunction in Neurodegeneration and Its Effects on Lipid Metabolism, Calcium Signaling, and Cell Fate.Membranes · 2025Review
- Article
- Exercise Empowerment: A Multifaceted Anatomy in Managing Diabetic Myocardial Disorder.Journal of cardiovascular translational research · 2025Review
- Menstrual cycle influence on skeletal muscle mitochondrial respiration in humans.Physiological reports · 2025Article
- Bypassing the guardian: regulated cell death pathways in p53-mutant cancers.Cellular & molecular biology letters · 2025Review
136 more citing papers are in PubMed but not listed here.
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Calcium is believed to regulate mitochondrial oxidative phosphorylation, thereby contributing to the maintenance of cellular energy homeostasis. Skeletal muscle, with an energy conversion dynamic range of up to 100-fold, is an extreme case for evaluating the cellular balance of ATP production and consumption. This study examined the role of Ca(2+) in the entire oxidative phosphorylation reaction network in isolated skeletal muscle mitochondria and attempted to extrapolate these results back to the muscle, in vivo. Kinetic analysis was conducted to evaluate the dose-response effect of Ca(2+) on the maximal velocity of oxidative phosphorylation (V(maxO)) and the ADP affinity. Force-flow analysis evaluated the interplay between energetic driving forces and flux to determine the conductance, or effective activity, of individual steps within oxidative phosphorylation. Measured driving forces [extramitochondrial phosphorylation potential (ΔG(ATP)), membrane potential, and redox states of NADH and cytochromes b(H), b(L), c(1), c, and a,a(3)] were compared with flux (oxygen consumption) at 37 °C; 840 nM Ca(2+) generated an ~2-fold increase in V(maxO) with no change in ADP affinity (~43 μM). Force-flow analysis revealed that Ca(2+) activation of V(maxO) was distributed throughout the oxidative phosphorylation reaction sequence. Specifically, Ca(2+) increased the conductance of Complex IV (2.3-fold), Complexes I and III (2.2-fold), ATP production/transport (2.4-fold), and fuel transport/dehydrogenases (1.7-fold). These data support the notion that Ca(2+) activates the entire muscle oxidative phosphorylation cascade, while extrapolation of these data to the exercising muscle predicts a significant role of Ca(2+) in maintaining cellular energy homeostasis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.