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

被引:207
作者
Buford, Thomas W. [1 ]
Anton, Stephen D.
Judge, Andrew R.
Marzetti, Emanuele
Wohlgemuth, Stephanie E.
Carter, Christy S.
Leeuwenburgh, Christiaan
Pahor, Marco
Manini, Todd M. [1 ]
机构
[1] Univ Florida, Dept Aging & Geriatr Res, Inst Aging, Gainesville, FL 32611 USA
关键词
Aging; Proteolysis; Satellite cells; HIV; COPD; Disability; UBIQUITIN-PROTEASOME PATHWAY; RESTING ENERGY-EXPENDITURE; NECROSIS-FACTOR-ALPHA; HUMAN SKELETAL-MUSCLE; GROWTH-FACTOR-I; LEAN BODY-MASS; ACQUIRED-IMMUNODEFICIENCY-SYNDROME; MYOFIBRILLAR PROTEIN-SYNTHESIS; PERIPHERAL ARTERIAL-DISEASE; AMINO-ACID SUPPLEMENTATION;
D O I
10.1016/j.arr.2010.04.004
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
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. (C) 2010 Elsevier B.V. All rights reserved.
引用
收藏
页码:369 / 383
页数:15
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