Asset Details
Do you wish to reserve the book?
Mitochondrial calcium uptake
Hey, we have placed the reservation for you!
By the way, why not check out events that you can attend while you pick your title.
Oops! Something went wrong.
Looks like we were not able to place the reservation. Kindly try again later.
Are you sure you want to remove the book from the shelf?
Mitochondrial calcium uptake
Do you wish to request the book?
Mitochondrial calcium uptake
Please be aware that the book you have requested cannot be checked out. If you would like to checkout this book, you can reserve another copy
We have requested the book for you!
Your request is successful and it will be processed during the Library working hours. Please check the status of your request in My Requests.
Oops! Something went wrong.
Looks like we were not able to place your request. Kindly try again later.
Journal Article
Mitochondrial calcium uptake
2013
Overview
Calcium (Ca²⁺) uptake into the mitochondrial matrix is critically important to cellular function. As a regulator of matrix Ca²⁺ levels, this flux influences energy production and can initiate cell death. If large, this flux could potentially alter intracellular Ca²⁺ ([Ca²⁺]i) signals. Despite years of study, fundamental disagreements on the extent and speed of mitochondrial Ca²⁺ uptake still exist. Here, we review and quantitatively analyze mitochondrial Ca²⁺ uptake fluxes from different tissues and interpret the results with respect to the recently proposed mitochondrial Ca²⁺ uniporter (MCU) candidate. This quantitative analysis yields four clear results: (i) under physiological conditions, Ca²⁺ influx into the mitochondria via the MCU is small relative to other cytosolic Ca²⁺ extrusion pathways; (ii) single MCU conductance is ~6-7 pS (105 mM [Ca²⁺]), and MCU flux appears to be modulated by [Ca²⁺]i, suggesting Ca²⁺ regulation of MCU open probability (Po); (iii) in the heart, two features are clear: the number of MCU channels per mitochondrion can be calculated, and MCU probability is low under normal conditions; and (iV) in skeletal muscle and liver cells, uptake per mitochondrion varies in magnitude but total uptake per cell still appears to be modest. Based on our analysis of available quantitative data, we conclude that although Ca²⁺ critically regulates mitochondrial function, the mitochondria do not act as a significant dynamic buffer of cytosolic Ca²⁺ under physiological conditions. Nevertheless, with prolonged (superphysiological) elevations of [Ca²⁺]i, mitochondrial Ca²⁺ uptake can increase 10- to 1,000-fold and begin to shape [Ca²⁺]i dynamics.
Publisher
National Academy of Sciences,National Acad Sciences
