ReviewBiomolecules2022
Calcium Overload and Mitochondrial Metabolism.
Review in Biomolecules, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
91 citing papers in PubMed.
- Effects of different arterial occlusion pressures during blood flow restriction exercise on muscle damage: a single-blind randomized controlled trial.Scientific reports · 2025Trial
- Mechanisms and therapeutic potential of mitochondrial-targeted therapies in bone repair.Annals of medicine · 2026Review
- Pioneering next-generation bioactive materials for endodontics: Insights of mitochondrial biology.Bioactive materials · 2026Article
- Mitochondrial calcium and ROS: present understanding and future directions.Mitochondrion · 2026Article
- Interplay between store-operated calcium entry and mitochondrial phosphate handling modulates force and fatigue during exercise.The Journal of physiology · 2026Article
- Docosahexaenoic acid alleviates Ornidazole toxicity related to spermatogenic dysfunction by modulating PPARγ-dependent ER-mitochondrial uncoupling.Science China. Life sciences · 2026Article
- Ion-Driven Regulation of CaAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Mitochondrial Cristae as Separate Compartments: Linking Organization and Function.Current issues in molecular biology · 2026Review
- Three-dimensional printed PCL/nHA scaffolds promote soft tissue functional fibrosis to repair chest wall defect via Piezo1/CaBioactive materials · 2026Article
- Identification and preliminary examination of prognostic genes linked to calcium metabolism in colorectal cancer.Journal of gastrointestinal oncology · 2026Article
- The two faces of mitochondrial CaJournal of physiology and biochemistry · 2026Review
- Review
- Review
- Scutellaria baicalensis exosome-like nanoparticles combat lung infection caused by Mycoplasma gallisepticum by regulating calcium homeostasis.Journal of animal science and biotechnology · 2026Article
- Extracellular vesicles: Revolutionizing targeted therapy for ischemic stroke.Acta pharmaceutica Sinica. B · 2026Review
- Ageing-Dependent Thyroid Hormone Receptor α Reduction Activates IP3R1-Meditated CaCell proliferation · 2026Article
- Shengmai San Ameliorates High-Glucose-Induced Calcium Homeostasis Imbalance via Improving Energy Metabolism in Neonatal Rat Cardiomyocytes.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Calcium Disorders in Rheumatic Diseases: An Overlooked Problem With Major Clinical Implications.Cureus · 2026Review
- Article
- The PVAT-MAMs Axis in Atherosclerosis: A Hypothesis-Driven Cross-Scale Conceptual Framework.International journal of molecular sciences · 2026Review
31 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
Abstract
Mitochondria calcium is a double-edged sword. While low levels of calcium are essential to maintain optimal rates of ATP production, extreme levels of calcium overcoming the mitochondrial calcium retention capacity leads to loss of mitochondrial function. In moderate amounts, however, ATP synthesis rates are inhibited in a calcium-titratable manner. While the consequences of extreme calcium overload are well-known, the effects on mitochondrial function in the moderately loaded range remain enigmatic. These observations are associated with changes in the mitochondria ultrastructure and cristae network. The present mini review/perspective follows up on previous studies using well-established cryo-electron microscopy and poses an explanation for the observable depressed ATP synthesis rates in mitochondria during calcium-overloaded states. The results presented herein suggest that the inhibition of oxidative phosphorylation is not caused by a direct decoupling of energy metabolism via the opening of a calcium-sensitive, proteinaceous pore but rather a separate but related calcium-dependent phenomenon. Such inhibition during calcium-overloaded states points towards mitochondrial ultrastructural modifications, enzyme activity changes, or an interplay between both events.
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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.