Mitochondrial function in cardiomyocytes: target for cardioprotection.
OBJECTIVE
Cardiac diseases including ischemic heart disease, cardiomyopathy, hypertension, atherosclerosis and congestive heart failure are associated with cardiac cell death as a result of both necrosis and apoptosis. Mitochondria play an essential role in deciding whether a cell lives or dies. This review summarizes current knowledge on the mechanisms by which mitochondria exert such decision-making power.


RESULTS
A wide variety of factors, either directly or indirectly, function in a synchronized manner to regulate the death versus survival signals. Mitochondrial bioenergetics and permeability transition pore plays a crucial role in this process, although several redox-sensitive genes, proteins and transcription factors, such as Bcl-2, Bax, nuclear factor kappa B, regulate the decision-making power of mitochondria, which have the final authority to decide whether a cell lives or dies. Mitochondrially generated reactive oxygen species are critically involved in the decision-making process, by functioning both as executioner by damaging the biomolecules, or as savior by virtue of their ability to perform redox signaling.


CONCLUSIONS
It appears that mitochondria regulate the life and death of cardiac cells by manipulating several factors, including bioenergetics, mitochondrial permeability transition pore and redox-sensing genes. Redox signaling is likely to be critically involved in this process.
Das
Dipak K
DK
Cardiovascular Research Center, University of Connecticut School of Medicine, Farmington, Connecticut 06030-1110, USA. ddas@neuron.uchc.edu
Maulik
Nilanjana
N