Calcium, ATP, and ROS: a mitochondrial love-hate triangle.

By P. Brookes, Y. Yoon, J. Robotham, M. W. Anders, S. Sheu. American Journal of Physiology - Cell Physiology, 2004

2,600 citations recorded by the source corpus.

Subfields: Clinical Biochemistry, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/c29ea225b1e356b1ec79f012062748d60fc9333a

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Clinical Biochemistry

In Molecular Biology

Citations in the corpus

Hallmarks of neurodegenerative diseases. (2023, neutral): “198 Reduced mitochondrial function and ATP synthesis is also associated with lower production of the scavenger glutathione (GSH), potentially worsening the oxidative environment of the cell.”
Initiation and perpetuation of NLRP3 inflammasome activation and assembly (2015, background): “Through normal respiratory functions mitochondria produce mitochondrial ROS (mtROS), but under stress mtROS production can increase enormously (102, 103).”
Fuel feeds function: energy metabolism and the T-cell response (2005, background): “Cytosolic Ca 2+ is then actively transported into the mitochondrion, where it stimulates the global rate of oxidative phosphorylation, in part by allosterically activating several key enzymes such as pyruvate dehydrogenase and ATP synthas”
Molecular Mechanisms of Ischemia-Reperfusion Injury in Brain: Pivotal Role of the Mitochondrial Membrane Potential in Reactive Oxygen Species Generation (2012, background): “Indeed, others have questioned how a normal physiologic stimulus to increase energy production can lead to a pathologic increase in ROS generation [88].”
Comparison of the Mechanism of Toxicity of Zinc Oxide and Cerium Oxide Nanoparticles Based on Dissolution and Oxidative Stress Properties (2008, positive): “This increase in the [Ca(2) ]i originates from intracellular storage sites such as the endoplasmic reticulum.(44,45) ZnO exposure induced a significant and sustained [Ca(2) ]i increase in both cell types as determined by Fluo-4 fluorescence (Figures 4C and 5C).”
Potential Role of Carotenoids as Antioxidants in Human Health and Disease (2014, background): “The most common include cancer, cardiovascular diseases, photosensitivity disorders, diabetes, neurological disorders or various types of inflammation, as well as processes correlated with ageing (Figure 3) [48,82–84].”
The inflammasome: an integrated view (2011, background): “Mitochondria constitutively produce low amounts of ROS, but stress conditions or disturbance of the respiratory chain can lead to an increased production of these molecules (105).”
Mitochondrial dysfunction and molecular pathways of disease. (2007, background): “Electrons donated from NADH and FADH flow through the ETC complexes, passing down an electrochemical gradient to be delivered to diatomic oxygen (O2) via a chain of respiratory proton (H) pumps (Brookes et al., 2004).”
Common mechanisms of amyloid oligomer pathogenesis in degenerative disease. (2006, background): “[9] Brookes PS, Yoon Y, Robotham JL, Anders MW, Sheu SS.”
Acrolein: sources, metabolism, and biomolecular interactions relevant to human health and disease. (2008, background): “Using biotin-tagged 15d-PGJ 2 , Darley-Usmar and colleagues were able to identify several putative mitochondrial protein targets of 15d-PGJ 2 , two of which seem to be particularly relevant to the opening of the PTP, i.e ., ANT (adenine nucleotide translocase) and ATP synthase [132].”
Cell death by necrosis: towards a molecular definition. (2007, background): “presumably because of the existence of self-destructive feed-forward loops [ 12 ].”
Superoxide Flashes in Single Mitochondria (2008, neutral): “Depending on concentration, location and context, ROS can be either ‘‘friends’’ or ‘‘foes.’’ Excessive ROS generation leads to apoptotic and necrotic cell death ( Brookes et al., 2004; Dypbukt et al., 1994) and pathogenesis of a panel of clinically distinct disorders including neurodegeneration (e.”
Mitochondrial Glutathione, a Key Survival Antioxidant (2009, background): “regulation of glutathione protects neurons against Abeta (1-42)-mediated oxidative stress and neurotoxicity: implica-”