Models of accelerated sarcopenia: Critical pieces for solving the puzzle of age-related muscle atrophy

Abstract Sarcopenia, the age-related loss of skeletal muscle mass, is a significant public health concern that continues to grow in relevance as the population ages. Certain conditions have the strong potential to coincide with sarcopenia to accelerate the progression of muscle atrophy in older adul...

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Bibliographic Details
Published in:Ageing research reviews Vol. 9; no. 4; pp. 369 - 383
Main Authors: Buford, Thomas W, Anton, Stephen D, Judge, Andrew R, Marzetti, Emanuele, Wohlgemuth, Stephanie E, Carter, Christy S, Leeuwenburgh, Christiaan, Pahor, Marco, Manini, Todd M
Format: Journal Article
Language:English
Published: England 01-10-2010
Subjects:
UCP
DM
MHC
UPS
AIF
IL
ROS
CNF
SC
NPY
GC
CKD
CI
PMC
PAD
HIV
PEM
HF
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Summary:Abstract Sarcopenia, the age-related loss of skeletal muscle mass, is a significant public health concern that continues to grow in relevance as the population ages. Certain conditions have the strong potential to coincide with sarcopenia to accelerate the progression of muscle atrophy in older adults. Among these conditions are co-morbid diseases common to older individuals such as cancer, kidney disease, diabetes, and peripheral artery disease. Furthermore, behaviors such as poor nutrition and physical inactivity are well-known to contribute to sarcopenia development. However, we argue that these behaviors are not inherent to the development of sarcopenia but rather accelerate its progression. In the present review, we discuss how these factors affect systemic and cellular mechanisms that contribute to skeletal muscle atrophy. In addition, we describe gaps in the literature concerning the role of these factors in accelerating sarcopenia progression. Elucidating biochemical pathways related to accelerated muscle atrophy may allow for improved discovery of therapeutic treatments related to sarcopenia.
Bibliography:ObjectType-Article-2
SourceType-Scholarly Journals-1
ObjectType-Feature-3
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ObjectType-Review-1
ISSN:1568-1637
1872-9649
DOI:10.1016/j.arr.2010.04.004