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Desmin cytoskeleton: A potential regulator of muscle mitochondrial behavior and function

Journal

TRENDS IN CARDIOVASCULAR MEDICINE
Volume 12, Issue 8, Pages 339-348

Publisher

ELSEVIER SCIENCE LONDON
DOI: 10.1016/S1050-1738(02)00184-6

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Funding

  1. NIAMS NIH HHS [AR39617] Funding Source: Medline

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Alterations in mitochondrial distribution and morphology are associated with normal cellular processes such as cell division and differentiation, as well as a variety of pathological conditions, including muscular dystrophy and cardiomyopathy. These observations have illuminated the necessity for a cellular machinery that mediates mitochondrial behavior and function. One important candidate member of this machinery is the cytoskeleton, all three members of which seem to associate with mitochondria. The role and significance of such association with the intermediate filament (IF) cytoskeleton in muscle was until recently completely unknown. Recent studies with desmin-deficient mice revealed the importance of desmin IFs in mitochondrial behavior and function. This review summarizes recent findings that link desmin cytoskeleton to muscle mitochondrial distribution and function. In particular, hypotheses are presented on the potential mechanism by which desmins absence from cardiac muscle leads to abnormal mitochondrial behavior and compromised function, potentially responsible for the development of dilated cardiomyopathy and heart failure in desmin-null mice. (C) 2002, Elsevier Science Inc.

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