Abstract
PURPOSE OF REVIEW: There are a variety of pathophysiologic conditions that are known to induce skeletal muscle atrophy. However, muscle wasting can occur through multiple distinct signaling pathways with differential sensitivity between selective skeletal muscle fiber subtypes. This review summarizes some of the underlying molecular mechanisms responsible for fiber-specific muscle mass regulation. RECENT FINDINGS: Peroxisome proliferator-activated receptor gamma coactivator 1-alpha protects slow-twitch oxidative fibers from denervation/immobilization (disuse)-induced muscle atrophies. Nutrient-related muscle atrophies, such as those induced by cancer cachexia, sepsis, chronic heart failure, or diabetes, are largely restricted to fast-twitch glycolytic fibers, of which the underlying mechanism is usually related to abnormality of protein degradation, including proteasomal and lysosomal pathways. In contrast, nuclear factor kappaB activation apparently serves a dual function by inducing both fast-twitch fiber atrophy and slow-twitch fiber degeneration. SUMMARY: Fast-twitch glycolytic fibers are more vulnerable than slow-twitch oxidative fibers under a variety of atrophic conditions related to signaling transduction of Forkhead box O family, autophagy inhibition, transforming growth factor beta family, and nuclear factor-kappaB. The resistance of oxidative fibers may result from the protection of peroxisome proliferator-activated receptor gamma coactivator 1-alpha.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 243-250 |
| Number of pages | 8 |
| Journal | Current Opinion in Clinical Nutrition and Metabolic Care |
| Volume | 16 |
| Issue number | 3 |
| DOIs | |
| State | Published - May 2013 |
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Keywords
- fiber-specific atrophy
- signaling
- skeletal muscle
ASJC Scopus subject areas
- Medicine (miscellaneous)
- Nutrition and Dietetics
Cite this
Mechanisms for fiber-type specificity of skeletal muscle atrophy. / Wang, Yichen; Pessin, Jeffrey E.
In: Current Opinion in Clinical Nutrition and Metabolic Care, Vol. 16, No. 3, 05.2013, p. 243-250.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Mechanisms for fiber-type specificity of skeletal muscle atrophy
AU - Wang, Yichen
AU - Pessin, Jeffrey E.
PY - 2013/5
Y1 - 2013/5
N2 - PURPOSE OF REVIEW: There are a variety of pathophysiologic conditions that are known to induce skeletal muscle atrophy. However, muscle wasting can occur through multiple distinct signaling pathways with differential sensitivity between selective skeletal muscle fiber subtypes. This review summarizes some of the underlying molecular mechanisms responsible for fiber-specific muscle mass regulation. RECENT FINDINGS: Peroxisome proliferator-activated receptor gamma coactivator 1-alpha protects slow-twitch oxidative fibers from denervation/immobilization (disuse)-induced muscle atrophies. Nutrient-related muscle atrophies, such as those induced by cancer cachexia, sepsis, chronic heart failure, or diabetes, are largely restricted to fast-twitch glycolytic fibers, of which the underlying mechanism is usually related to abnormality of protein degradation, including proteasomal and lysosomal pathways. In contrast, nuclear factor kappaB activation apparently serves a dual function by inducing both fast-twitch fiber atrophy and slow-twitch fiber degeneration. SUMMARY: Fast-twitch glycolytic fibers are more vulnerable than slow-twitch oxidative fibers under a variety of atrophic conditions related to signaling transduction of Forkhead box O family, autophagy inhibition, transforming growth factor beta family, and nuclear factor-kappaB. The resistance of oxidative fibers may result from the protection of peroxisome proliferator-activated receptor gamma coactivator 1-alpha.
AB - PURPOSE OF REVIEW: There are a variety of pathophysiologic conditions that are known to induce skeletal muscle atrophy. However, muscle wasting can occur through multiple distinct signaling pathways with differential sensitivity between selective skeletal muscle fiber subtypes. This review summarizes some of the underlying molecular mechanisms responsible for fiber-specific muscle mass regulation. RECENT FINDINGS: Peroxisome proliferator-activated receptor gamma coactivator 1-alpha protects slow-twitch oxidative fibers from denervation/immobilization (disuse)-induced muscle atrophies. Nutrient-related muscle atrophies, such as those induced by cancer cachexia, sepsis, chronic heart failure, or diabetes, are largely restricted to fast-twitch glycolytic fibers, of which the underlying mechanism is usually related to abnormality of protein degradation, including proteasomal and lysosomal pathways. In contrast, nuclear factor kappaB activation apparently serves a dual function by inducing both fast-twitch fiber atrophy and slow-twitch fiber degeneration. SUMMARY: Fast-twitch glycolytic fibers are more vulnerable than slow-twitch oxidative fibers under a variety of atrophic conditions related to signaling transduction of Forkhead box O family, autophagy inhibition, transforming growth factor beta family, and nuclear factor-kappaB. The resistance of oxidative fibers may result from the protection of peroxisome proliferator-activated receptor gamma coactivator 1-alpha.
KW - fiber-specific atrophy
KW - signaling
KW - skeletal muscle
UR - http://www.scopus.com/inward/record.url?scp=84876414410&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84876414410&partnerID=8YFLogxK
U2 - 10.1097/MCO.0b013e328360272d
DO - 10.1097/MCO.0b013e328360272d
M3 - Article
C2 - 23493017
AN - SCOPUS:84876414410
VL - 16
SP - 243
EP - 250
JO - Current Opinion in Clinical Nutrition and Metabolic Care
JF - Current Opinion in Clinical Nutrition and Metabolic Care
SN - 1363-1950
IS - 3
ER -