Related Experiment Video
Updated: May 31, 2026

A Flow Cytometry-based Assay for Measuring Mitochondrial Membrane Potential in Cardiac Myocytes After Hypoxia/Reoxygenation
Published on: July 13, 2018
The role of mitochondrial membrane potential in ischemic heart failure
Bernhard Kadenbach1, Rabia Ramzan, Rainer Moosdorf
1Fachbereich Chemie, Philipps-Universitaet, D-35032 Marburg, Germany. kadenbach@staff.uni-marburg.de
Abstract:
The molecular events occurring during myocardial infarction and cardioprotection are described with an emphasis on the changes of the mitochondrial membrane potential (ΔΨ(m)). The low ΔΨ(m) values of the normal beating heart (100-140 mV) are explained by the allosteric ATP-inhibition of cytochrome c oxidase (CcO) through feedback inhibition by ATP at high [ATP]/[ADP] ratios. During ischemia the mechanism is reversibly switched off by signaling through reactive oxygen species (ROS). At reperfusion high ΔΨ(m) values cause a burst of ROS production leading to apoptosis and/or necrosis. Ischemic preconditioning is suggested to cause additional phosphorylation of CcO, protecting the enzyme from immediate dephosphorylation via ROS signaling.
Related Concept Videos
Pathophysiology of Heart Failure
Heart Failure II: Pathophysiology
Mitochondrial Membranes
Mitochondrial Membranes
The Inner Mitochondrial Membrane
Heart Failure I: Introduction
