Abstract
Over the past 10 years, mitochondrial defects have been implicated in a wide variety of degenerative diseases, aging, and cancer. Studies on patients with these diseases have revealed much about the complexities of mitochondrial genetics, which involves an interplay between mutations in the mitochondrial and nuclear genomes. However, the pathophysiology of mitochondrial diseases has remained perplexing. The essential role of mitochondrial oxidative phosphorylation in cellular energy production, the generation of reactive oxygen species, and the initiation of apoptosis has suggested a number of novel mechanisms for mitochondrial pathology. The importance and interrelationship of these functions are now being studied in mouse models of mitochondrial disease.
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- I thank my colleagues at the Center for Molecular Medicine who participated in this work. In alphabetical order these include: J. Bilgar M. Brown R. Burke P. Coskun B. Cottrell L. Esposito P. Hatten-Mitchell J. Kokoszak S. Levy M. Lott G. MacGregor S. Melov D. Murdock J. Petros C. Stugard J. Sligh and K. Waymire. Supported by NIH grants HL45572 AG13154 and NS21328 and by a Johnson and Johnson Focused Giving Grant.
Dates
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Created | 23 years, 1 month ago (July 27, 2002, 5:48 a.m.) |
Deposited | 1 year, 7 months ago (Jan. 13, 2024, 12:06 a.m.) |
Indexed | 5 minutes ago (Sept. 4, 2025, 6:24 a.m.) |
Issued | 26 years, 5 months ago (March 5, 1999) |
Published | 26 years, 5 months ago (March 5, 1999) |
Published Print | 26 years, 5 months ago (March 5, 1999) |