Publication Date:
1999-03-05
Description:
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.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wallace, D C -- AG13154/AG/NIA NIH HHS/ -- HL45572/HL/NHLBI NIH HHS/ -- NS21328/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1999 Mar 5;283(5407):1482-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Molecular Medicine, Emory University, 1462 Clifton Road, Suite 420, Atlanta, GA 30322, USA. dwallace@gmm.gen.emory.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10066162" target="_blank"〉PubMed〈/a〉
Keywords:
Aging/genetics
;
Animals
;
DNA, Mitochondrial/*genetics
;
Humans
;
Metabolic Diseases/*genetics/metabolism
;
Mice
;
Mitochondria/*genetics/metabolism
;
Mitochondrial Myopathies/*genetics/metabolism
;
Mutation
;
Neoplasms/genetics/metabolism
;
Oxidative Phosphorylation
Print ISSN:
0036-8075
Electronic ISSN:
1095-9203
Topics:
Biology
,
Chemistry and Pharmacology
,
Computer Science
,
Medicine
,
Natural Sciences in General
,
Physics
