ReviewJournal of bioenergetics and biomembranes2009
Regulation of mitochondrial Ca2+ and its effects on energetics and redox balance in normal and failing heart.
Review in Journal of bioenergetics and biomembranes, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
57 citing papers in PubMed, 98 citations in OpenAlex.
- Structural and Functional Regulation of RyR2 in Cardiac Calcium Handling and Arrhythmogenesis.Biomedicines · 2026Review
- Calcium Signaling and Cardiac Adaptation to Stress: Focus on Pregnancy and Diabetes.Biomolecules · 2025Review
- Crosstalk between calcium and reactive oxygen species signaling in cancer revisited.Cell calcium · 2025Review
- Inter- and intracellular mitochondrial communication: signaling hubs in aging and age-related diseases.Cellular & molecular biology letters · 2024Review
- Bag3 Regulates Mitochondrial Function and the Inflammasome Through Canonical and Noncanonical Pathways in the Heart.JACC. Basic to translational science · 2023Article
- BAG3: Nature's Quintessential Multi-Functional Protein Functions as a Ubiquitous Intra-Cellular Glue.Cells · 2023Review
- Review
- Testosterone deficiency impairs cardiac interfibrillar mitochondrial function and myocardial contractility while inducing oxidative stress.Frontiers in endocrinology · 2023Article
- The Therapeutic Strategies Targeting Mitochondrial Metabolism in Cardiovascular Disease.Pharmaceutics · 2022Review
- Neurohormonal connections with mitochondria in cardiomyopathy and other diseases.American journal of physiology. Cell physiology · 2022Review
- Digitoxin Affects Metabolism, ROS Production and Proliferation in Pancreatic Cancer Cells Differently Depending on the Cell Phenotype.International journal of molecular sciences · 2022Article
- MCU Overexpression Rescues Inotropy and Reverses Heart Failure by Reducing SR CaCirculation research · 2021Article
- TNFα induces mitochondrial fragmentation and biogenesis in human airway smooth muscle.American journal of physiology. Lung cellular and molecular physiology · 2021Article
- Increased RyR2 activity is exacerbated by calcium leak-induced mitochondrial ROS.Basic research in cardiology · 2020Article
- Review
- Role of Mitochondrial Calcium and the Permeability Transition Pore in Regulating Cell Death.Circulation research · 2020Review
- Regulation of Mitochondrial ATP Production: CaTrends in molecular medicine · 2020Review
- Sarcoplasmic Reticulum-Mitochondria Kissing in Cardiomyocytes: CaFrontiers in cell and developmental biology · 2020Review
- miR-181c Activates Mitochondrial Calcium Uptake by Regulating MICU1 in the Heart.Journal of the American Heart Association · 2019Article
- Genetically targeted fluorescent probes reveal dynamic calcium responses to adrenergic signaling in multiple cardiomyocyte compartments.The international journal of biochemistry & cell biology · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Ca(2+) has been well accepted as a signal that coordinates changes in cytosolic workload with mitochondrial energy metabolism in cardiomyocytes. During increased work, Ca(2+) is accumulated in mitochondria and stimulates ATP production to match energy supply and demand. The kinetics of mitochondrial Ca(2+) ([Ca(2+)](m)) uptake remains unclear, and we review the debate on this subject in this article. [Ca(2+)](m) has multiple targets in oxidative phosphorylation including the F1/FO ATPase, the adenine nucleotide translocase, and Ca(2+)-sensitive dehydrogenases (CaDH) of the tricarboxylic acid (TCA) cycle. The well established effect of [Ca(2+)](m) is to activate CaDHs of the TCA cycle to increase NADH production. Maintaining NADH level is not only critical to keep a high oxidative phosphorylation rate during increased cardiac work, but is also necessary for the reducing system of the cell to maintain its reactive oxygen species (ROS) -scavenging capacity. Further, we review recent data demonstrating the deleterious effects of elevated Na(+) in cardiac pathology by blunting [Ca(2+)](m) accumulation.
Indexed as
Identifiers
What OpenQuestion holds
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.