Original scientific paper
CARDIOPROTECTION BY PRE- AND POST-CONDITIONING: IMPLICATIONS FOR THE ROLE OF MITOCHONDRIA
AKS Camara
; Department of Anesthesiology and Anesthesia Research Medical College of Wisconsin, Milwaukee, WI 53226
M Aldakkak
; Department of Anesthesiology and Anesthesia Research Medical College of Wisconsin, Milwaukee, WI 53226
Martin Bienengraeber
; Department of Anesthesiology and Anesthesia Research Medical College of Wisconsin, Milwaukee, WI 53226
DF Stowe
; Department of Anesthesiology and Anesthesia Research Medical College of Wisconsin, Milwaukee, WI 53226
Abstract
The mitochondrion has evolved as an important organelle in
determining cell survival and cell death. It is involved in a plethora of processes
in mammalian cells including ATP production, steroid synthesis, and
cell division and cell death. Indeed, mitochondrial dysfunction is associated
with numerous human maladies including heart disease. Mitochondrial
diseases have traditionally been attributed to defects in the electron transport
chain (ETC), the major source of mitochondrial reactive oxygen species
(ROS), a byproduct of mitochondrial respiration. Mitochondrial cation
channels and exchangers function to maintain matrix homeostasis and are
likely involved in modulating mitochondrial function in part by regulating
O2
•- generation. Insofar as mitochondria are involved in oxidative damage
that leads to apoptosis, antioxidants and other therapeutic strategies
that target the organelle appear to be a novel approach to alleviate some
cardiovascular diseases. This novel approach has gained unprecedented
attention recently with a significant potential for future therapeutic purpose.
Whether mitochondria are targets or end effectors of cardiac pre- and
post-conditioning remain unresolved. This brief review will provide the latest
information gleaned from the literature on the role of mitochondria in
pre- and post-conditioning during cardiac ischemia and reperfusion.
Keywords
Hrčak ID:
70920
URI
Publication date:
27.5.2011.
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