Network Dynamics in Cardiac Electrophysiology - Systems Biology of Metabolic and Signaling Networks - page 243

a

time (s) p =0.25 p =0.30 p =0.40 p =0.60

0
2.5

5
7.5
10

20 mm

SO C (mM)

0 0.02 0.04 0.06

b c

p=0.25

p=0.3

p=0.4

time

100 s

Log(cluster size)

Fig. 10.5 Transition from flickers to waves in a mitochondrial network .(a) Snapshots of super-
oxide concentration in the cytoplasmic space at five time points and for different p .(b) Mitochon-
drial depolarization Cluster size distribution for different p .(c) Whole-cell mitochondrial potential
versus time for different p

potential changes from exhibiting small random fluctuations to more periodic
oscillations as superoxide production rate increases (Fig. 10.5c ).
Since when criticality is reached, a random flicker may cause a cascade event,
triggering a macroscopic mitochondrial depolarization event. The massive mito-
chondrial depolarization consumes ATP to a low level that opens the K ATP
channels, shortening the action potential. In other words, at criticality, a random
single mitochondrial event may cause a macroscopic cellular event at the cellular
level, which may trigger a sudden arrhythmia event at the tissue scale.

10.3 Cellular Electrophysiology: Dynamics from
a Network of Networks

A cell is a network composed of molecular and organelle networks. The ionic
currents generated by the ion channels and Ca 2+ cycling regulate the excitation
dynamics, Ca 2+

cycling and the myofilament network generate the force for