Mitochondrial function in cardiomyocytes: target for cardioprotection.

Abstract

PURPOSE OF REVIEW: 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. RECENT FINDINGS: 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. SUMMARY: 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.