Muscle Atrophy Induced by Mechanical Unloading: Mechanisms and Potential Countermeasures

Prolonged periods of skeletal muscle inactivity or mechanical unloading (bed rest, hindlimb unloading, immobilization, spaceflight and reduced step) can result in a significant loss of musculoskeletal mass, size and strength which ultimately lead to muscle atrophy. With advancement in understanding...
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Autor*in:	Yunfang Gao [verfasserIn] Yasir Arfat [verfasserIn] Huiping Wang [verfasserIn] Nandu Goswami [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2018

Schlagwörter:	disuse muscle atrophy mechanical unloading protein synthesis protein degradation molecular and cellular pathways therapeutic countermeasures

Übergeordnetes Werk:	In: Frontiers in Physiology - Frontiers Media S.A., 2011, 9(2018)
Übergeordnetes Werk:	volume:9 ; year:2018

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.3389/fphys.2018.00235

Katalog-ID:	DOAJ027565114

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520			\|a Prolonged periods of skeletal muscle inactivity or mechanical unloading (bed rest, hindlimb unloading, immobilization, spaceflight and reduced step) can result in a significant loss of musculoskeletal mass, size and strength which ultimately lead to muscle atrophy. With advancement in understanding of the molecular and cellular mechanisms involved in disuse skeletal muscle atrophy, several different signaling pathways have been studied to understand their regulatory role in this process. However, substantial gaps exist in our understanding of the regulatory mechanisms involved, as well as their functional significance. This review aims to update the current state of knowledge and the underlying cellular mechanisms related to skeletal muscle loss during a variety of unloading conditions, both in humans and animals. Recent advancements in understanding of cellular and molecular mechanisms, including IGF1-Akt-mTOR, MuRF1/MAFbx, FOXO, and potential triggers of disuse atrophy, such as calcium overload and ROS overproduction, as well as their role in skeletal muscle protein adaptation to disuse is emphasized. We have also elaborated potential therapeutic countermeasures that have shown promising results in preventing and restoring disuse-induced muscle loss. Finally, identified are the key challenges in this field as well as some future prospectives.
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allfieldsSound	10.3389/fphys.2018.00235 doi (DE-627)DOAJ027565114 (DE-599)DOAJfbf9377d8aa0455cb86a3bee0db306b1 DE-627 ger DE-627 rakwb eng QP1-981 Yunfang Gao verfasserin aut Muscle Atrophy Induced by Mechanical Unloading: Mechanisms and Potential Countermeasures 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Prolonged periods of skeletal muscle inactivity or mechanical unloading (bed rest, hindlimb unloading, immobilization, spaceflight and reduced step) can result in a significant loss of musculoskeletal mass, size and strength which ultimately lead to muscle atrophy. With advancement in understanding of the molecular and cellular mechanisms involved in disuse skeletal muscle atrophy, several different signaling pathways have been studied to understand their regulatory role in this process. However, substantial gaps exist in our understanding of the regulatory mechanisms involved, as well as their functional significance. This review aims to update the current state of knowledge and the underlying cellular mechanisms related to skeletal muscle loss during a variety of unloading conditions, both in humans and animals. Recent advancements in understanding of cellular and molecular mechanisms, including IGF1-Akt-mTOR, MuRF1/MAFbx, FOXO, and potential triggers of disuse atrophy, such as calcium overload and ROS overproduction, as well as their role in skeletal muscle protein adaptation to disuse is emphasized. We have also elaborated potential therapeutic countermeasures that have shown promising results in preventing and restoring disuse-induced muscle loss. Finally, identified are the key challenges in this field as well as some future prospectives. disuse muscle atrophy mechanical unloading protein synthesis protein degradation molecular and cellular pathways therapeutic countermeasures Physiology Yasir Arfat verfasserin aut Huiping Wang verfasserin aut Nandu Goswami verfasserin aut In Frontiers in Physiology Frontiers Media S.A., 2011 9(2018) (DE-627)631498788 (DE-600)2564217-0 1664042X nnns volume:9 year:2018 https://doi.org/10.3389/fphys.2018.00235 kostenfrei https://doaj.org/article/fbf9377d8aa0455cb86a3bee0db306b1 kostenfrei http://journal.frontiersin.org/article/10.3389/fphys.2018.00235/full kostenfrei https://doaj.org/toc/1664-042X Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 9 2018
language	English
source	In Frontiers in Physiology 9(2018) volume:9 year:2018
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topic_facet	disuse muscle atrophy mechanical unloading protein synthesis protein degradation molecular and cellular pathways therapeutic countermeasures Physiology
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container_title	Frontiers in Physiology
authorswithroles_txt_mv	Yunfang Gao @@aut@@ Yasir Arfat @@aut@@ Huiping Wang @@aut@@ Nandu Goswami @@aut@@
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author	Yunfang Gao
spellingShingle	Yunfang Gao misc QP1-981 misc disuse muscle atrophy misc mechanical unloading misc protein synthesis misc protein degradation misc molecular and cellular pathways misc therapeutic countermeasures misc Physiology Muscle Atrophy Induced by Mechanical Unloading: Mechanisms and Potential Countermeasures
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topic_title	QP1-981 Muscle Atrophy Induced by Mechanical Unloading: Mechanisms and Potential Countermeasures disuse muscle atrophy mechanical unloading protein synthesis protein degradation molecular and cellular pathways therapeutic countermeasures
topic	misc QP1-981 misc disuse muscle atrophy misc mechanical unloading misc protein synthesis misc protein degradation misc molecular and cellular pathways misc therapeutic countermeasures misc Physiology
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title	Muscle Atrophy Induced by Mechanical Unloading: Mechanisms and Potential Countermeasures
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title_full	Muscle Atrophy Induced by Mechanical Unloading: Mechanisms and Potential Countermeasures
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title_sort	muscle atrophy induced by mechanical unloading: mechanisms and potential countermeasures
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title_auth	Muscle Atrophy Induced by Mechanical Unloading: Mechanisms and Potential Countermeasures
abstract	Prolonged periods of skeletal muscle inactivity or mechanical unloading (bed rest, hindlimb unloading, immobilization, spaceflight and reduced step) can result in a significant loss of musculoskeletal mass, size and strength which ultimately lead to muscle atrophy. With advancement in understanding of the molecular and cellular mechanisms involved in disuse skeletal muscle atrophy, several different signaling pathways have been studied to understand their regulatory role in this process. However, substantial gaps exist in our understanding of the regulatory mechanisms involved, as well as their functional significance. This review aims to update the current state of knowledge and the underlying cellular mechanisms related to skeletal muscle loss during a variety of unloading conditions, both in humans and animals. Recent advancements in understanding of cellular and molecular mechanisms, including IGF1-Akt-mTOR, MuRF1/MAFbx, FOXO, and potential triggers of disuse atrophy, such as calcium overload and ROS overproduction, as well as their role in skeletal muscle protein adaptation to disuse is emphasized. We have also elaborated potential therapeutic countermeasures that have shown promising results in preventing and restoring disuse-induced muscle loss. Finally, identified are the key challenges in this field as well as some future prospectives.
abstractGer	Prolonged periods of skeletal muscle inactivity or mechanical unloading (bed rest, hindlimb unloading, immobilization, spaceflight and reduced step) can result in a significant loss of musculoskeletal mass, size and strength which ultimately lead to muscle atrophy. With advancement in understanding of the molecular and cellular mechanisms involved in disuse skeletal muscle atrophy, several different signaling pathways have been studied to understand their regulatory role in this process. However, substantial gaps exist in our understanding of the regulatory mechanisms involved, as well as their functional significance. This review aims to update the current state of knowledge and the underlying cellular mechanisms related to skeletal muscle loss during a variety of unloading conditions, both in humans and animals. Recent advancements in understanding of cellular and molecular mechanisms, including IGF1-Akt-mTOR, MuRF1/MAFbx, FOXO, and potential triggers of disuse atrophy, such as calcium overload and ROS overproduction, as well as their role in skeletal muscle protein adaptation to disuse is emphasized. We have also elaborated potential therapeutic countermeasures that have shown promising results in preventing and restoring disuse-induced muscle loss. Finally, identified are the key challenges in this field as well as some future prospectives.
abstract_unstemmed	Prolonged periods of skeletal muscle inactivity or mechanical unloading (bed rest, hindlimb unloading, immobilization, spaceflight and reduced step) can result in a significant loss of musculoskeletal mass, size and strength which ultimately lead to muscle atrophy. With advancement in understanding of the molecular and cellular mechanisms involved in disuse skeletal muscle atrophy, several different signaling pathways have been studied to understand their regulatory role in this process. However, substantial gaps exist in our understanding of the regulatory mechanisms involved, as well as their functional significance. This review aims to update the current state of knowledge and the underlying cellular mechanisms related to skeletal muscle loss during a variety of unloading conditions, both in humans and animals. Recent advancements in understanding of cellular and molecular mechanisms, including IGF1-Akt-mTOR, MuRF1/MAFbx, FOXO, and potential triggers of disuse atrophy, such as calcium overload and ROS overproduction, as well as their role in skeletal muscle protein adaptation to disuse is emphasized. We have also elaborated potential therapeutic countermeasures that have shown promising results in preventing and restoring disuse-induced muscle loss. Finally, identified are the key challenges in this field as well as some future prospectives.
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title_short	Muscle Atrophy Induced by Mechanical Unloading: Mechanisms and Potential Countermeasures
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Muscle Atrophy Induced by Mechanical Unloading: Mechanisms and Potential Countermeasures

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