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Updated: Jul 8, 2026

Analyses of Mitochondrial Calcium Influx in Isolated Mitochondria and Cultured Cells

Analyses of Mitochondrial Calcium Influx in Isolated Mitochondria and Cultured Cells

Published on: April 27, 2018

Mitochondrial Ca2+ and the heart.

Elena N Dedkova¹, Lothar A Blatter

¹Department of Physiology, Loyola University Chicago, Stritch School of Medicine, 2160 S. First Avenue, Maywood, IL 60153, USA. ededkov@lumc.edu

|January 8, 2008

Summary

This summary is machine-generated.

Mitochondria take up calcium ions (Ca2+) during cell signaling. This review examines if cardiac mitochondria can rapidly transmit fast calcium changes, impacting cell energy and death.

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Analyses of Mitochondrial Calcium Influx in Isolated Mitochondria and Cultured Cells

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Mitochondrial Ca2+ Retention Capacity Assay and Ca2+-triggered Mitochondrial Swelling Assay

Mitochondrial Ca²⁺ Retention Capacity Assay and Ca²⁺-triggered Mitochondrial Swelling Assay

Published on: May 1, 2018

Area of Science:

Cellular Biology
Mitochondrial Physiology
Cardiovascular Research

Background:

Mitochondria accumulate cytosolic calcium (Ca2+) during elevations, influencing ATP production and cell death pathways.
Mitochondrial calcium uptake stimulates nitric oxide (NO) production, modulating energy metabolism and reactive oxygen species (ROS) generation.
NO provides negative feedback on mitochondrial calcium accumulation, highlighting complex regulatory mechanisms.

Purpose of the Study:

To critically review experimental evidence regarding mitochondrial calcium handling in cardiomyocytes.
To address the controversy surrounding beat-to-beat transmission of cytosolic calcium oscillations into mitochondria.

Main Methods:

Critical analysis of recent experimental studies on mitochondrial calcium dynamics.
Review of techniques used to measure intramitochondrial calcium ([Ca2+](m)) and cytosolic calcium ([Ca2+](i)) in cardiac myocytes.

Main Results:

Mitochondrial Ca2+ accumulation is established and impacts key cellular processes.
Evidence suggests complex interactions between mitochondrial Ca2+, NO, ATP production, and ROS.
The capacity for rapid, beat-to-beat mitochondrial Ca2+ oscillations in cardiomyocytes remains debated.

Conclusions:

Mitochondrial calcium plays a crucial role in cardiomyocyte function, energy metabolism, and cell fate.
Further research is needed to definitively resolve the question of rapid mitochondrial calcium signal transmission in cardiac myocytes.