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Official Journal of the Italian Society of Angiology and Vascular Pathology
Indexed/Abstracted in: EMBASE, PubMed/MEDLINE, Science Citation Index Expanded (SciSearch), Scopus
Impact Factor 0,752
Online ISSN 1827-1618
Chen L., Knowlton A. A.
1 Molecular and Cellular Cardiology, University of California, Davis, Davis, CA, USA;
2 V.A. Medical Center, Sacramento, CA, USA
Cardiac mitochondria are powerful organelles supplying energy to support the high adenosine triphosphate (ATP) consumption of the beating heart. The progression of HF (HF) is characterized by diminished energy metabolism, calcium mishandling, reactive oxygen species (ROS) generation and apoptotic cell death. Although the etiologies of HF are multifactoral, many of the changes of HF are associated with cardiac mitochondrial dysfunction either directly or indirectly. A number of studies have established the role of calcium mishandling and reduced ATP production in mitochondrial dysfunction in HF. More recent work has contributed to our understanding of the role of ROS and proapoptotic protein release by the mitochondria in HF. New interest has been generated in mitochondria by the relatively recent identification of the processes of fusion and fission, which are critical to the maintenance of healthy mitochondria. Fission and fusion also have significant roles in apoptosis. Other studies have shown that estrogen has important functions in the mitochondria, including regulation of mitochondrial gene expression. Aging alone contributes to the development of HF through multiple mechanisms. These new insights into HF have implications for our understanding of this important disease, and will be reviewed here.