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Genetic Deletion of Myostatin From the Heart Prevents Skeletal Muscle Atrophy in Heart Failure
Author(s) -
Joerg Heineke,
Mannix AugerMessier,
Jian Xu,
Michelle A. Sargent,
Allen J. York,
Stephen Welle,
Jeffery D. Molkentin
Publication year - 2010
Publication title -
circulation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.795
H-Index - 607
eISSN - 1524-4539
pISSN - 0009-7322
DOI - 10.1161/circulationaha.109.882068
Subject(s) - medicine , myostatin , heart failure , skeletal muscle , atrophy , cardiology , endocrinology
Cardiac cachexia is characterized by an exaggerated loss of skeletal muscle, weakness, and exercise intolerance, although the cause of these effects remains unknown. Here, we hypothesized that the heart functions as an endocrine organ in promoting systemic cachexia by secreting peptide factors such as myostatin. Myostatin is a cytokine of the transforming growth factor-beta superfamily that is known to control muscle wasting.

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