Mitochondria and calcium: from cell signalling to cell death

By M. Duchen. Journal of Physiology, 2000

1,281 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/88cfd4ad138898aa53f0bb71602da62b51076b1c

How researchers see this paper

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

In Cellular and Molecular Neuroscience

1. R. Balaban
2. B. Glancy
3. Mark P. Mattson
4. L. Galluzzi
5. M. Duchen
6. Guido Kroemer
7. A. Abramov
8. Michael T. Heneka

In Molecular Biology

1. Guido Kroemer
2. L. Galluzzi
3. M. Duchen
4. C. Brenner
5. A. Abramov
6. R. Balaban
7. B. Glancy
8. Mark P. Mattson

Citations in the corpus

• Mitochondrial membrane permeabilization in cell death. (2007, background): “hydrogenases) (188), to enhance metabolite flow on the”
• Calcium and neurodegeneration (2007, background): “Mark P. Mattson Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, Baltimore, MD, USA”
• Cellular and molecular mechanisms of mitochondrial function (2012, background): “1 Indeed, mitochondria have been referred to as ‘ poison cabinets ’ of the cell as key proteins released from the matrix and inner membrane initiate apoptotic cell death.”
• Redox Regulation of NLRP3 Inflammasomes: ROS as Trigger or Effector? (2015, neutral): “Excessive Ca(2) + can lead to an increase in mitochondrial ROS (mtROS) production, collapse of the mitochondrial membrane potential, and eventual mitochondria rupture (34).”
• β-Amyloid Peptides Induce Mitochondrial Dysfunction and Oxidative Stress in Astrocytes and Death of Neurons through Activation of NADPH Oxidase (2004, background): “The combined effect of high [Ca 2 ]c with oxidative stress may damage mitochondrial function and has been implicated as a pathophysiological mechanism in many systems (Duchen, 2000).”
• Calcium, ATP, and ROS: a mitochondrial love-hate triangle. (2004, background): “The mitochondrial Ca(2) hypothesis of excitotoxicity centers on [Ca(2) ]m overload as a central event in cell death (50, 135).”
• Role of Mitochondrial Ca2+ in the Regulation of Cellular Energetics (2012, methodology): “For the purposes of this review, we will assume that Cac influences Cam, though the temporal fidelity of this relationship may vary (see (29)).”