Calpain and caspase-3 play required roles in immobilization-induced limb muscle atrophy

Talbert, Erin E.; Smuder, Ashley J.; Min, Kisuk; Kwon, Oh Sung; Powers, Scott K.

doi:10.1152/japplphysiol.00925.2012

Cited by 81 publications

(64 citation statements)

References 31 publications

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“…This suggests that apoptosis would be a biological process promoting atrophy through a loss of myonuclei during immobilization. Such idea is supported by studies demonstrating that caspase-3 activity [59,89] and the apoptotic mitochondrial intrinsic pathways (i.e., endonuclease G and apoptosome) [86,90] are stimulated in unloaded skeletal muscle.…”

Section: Cellular Mechanisms Involved In Immobilization-induced Skelementioning

confidence: 92%

“…In skeletal muscle, recent studies demonstrated that both calpains and caspase-3 were activated by hindlimb unloading [59,95,96]. Interestingly, pharmacological inhibition of calpains or caspase-3 prevents type I fibers atrophy observed in casted rats, demonstrating that these proteases are mandatory for skeletal muscle atrophy [89].…”

Section: Cellular Mechanisms Involved In Immobilization-induced Skelementioning

confidence: 99%

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From physical inactivity to immobilization: Dissecting the role of oxidative stress in skeletal muscle insulin resistance and atrophy

Pierre

Appriou

Gratas-Delamarche

et al. 2016

Free Radical Biology and Medicine

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In the literature, the terms physical inactivity and immobilization are largely used as synonyms. The present review emphasizes the need to establish a clear distinction between these two situations. Physical inactivity is a behavior characterized by a lack of physical activity, whereas immobilization is a deprivation of movement for medical purpose. In agreement with these definitions, appropriate models exist to study either physical inactivity or immobilization, leading thereby to distinct conclusions. In this review, we examine the involvement of oxidative stress in skeletal muscle insulin resistance and atrophy induced by, respectively, physical inactivity and immobilization. A large body of evidence demonstrates that immobilization-induced atrophy depends on the chronic overproduction of reactive oxygen and nitrogen species (RONS). On the other hand, the involvement of RONS in physical inactivity-induced insulin resistance has not been investigated. This observation outlines the need to elucidate the mechanism by which physical inactivity promotes insulin resistance.

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Section: Cellular Mechanisms Involved In Immobilization-induced Skelementioning

confidence: 92%

Section: Cellular Mechanisms Involved In Immobilization-induced Skelementioning

confidence: 99%

From physical inactivity to immobilization: Dissecting the role of oxidative stress in skeletal muscle insulin resistance and atrophy

Pierre

Appriou

Gratas-Delamarche

et al. 2016

Free Radical Biology and Medicine

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show abstract

“…Although the causes of disuse-induced oxidative stress in skeletal muscle continues to be investigated, evidence suggests that prolonged skeletal muscle inactivity results in increased superoxide production at multiple locations in the cell including NAD(P)H oxidase, xanthine oxidase, and the mitochondria [20-24]. In regard to the relative contributions of each of these sources of ROS production, recent evidence suggests that mitochondria are a major source of ROS production in inactive skeletal muscles [20, 21, 25]. For example, compared to mitochondria obtained from skeletal muscles of active rodents, mitochondria from muscle exposed to prolonged periods of disuse release significantly more ROS [26] [20, 24].…”

Section: Sources Of Ros and Rns In Atrophying Skeletal Musclementioning

confidence: 99%

Redox control of skeletal muscle atrophy

Powers

Morton

Ahn

et al. 2016

Free Radical Biology and Medicine

Self Cite

149

157

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Skeletal muscles comprise the largest organ system in the body and play an essential role in body movement, breathing, and glucose homeostasis. Skeletal muscle is also an important endocrine organ that contributes to the health of numerous body organs. Therefore, maintaining healthy skeletal muscles is important to support overall health of the body. Prolonged periods of muscle inactivity (e.g., bed rest or limb immobilization) or chronic inflammatory diseases (i.e., cancer, kidney failure, etc.) result in skeletal muscle atrophy. An excessive loss of muscle mass is associated with a poor prognosis in several diseases and significant muscle weakness impairs the quality of life. The skeletal muscle atrophy that occurs in response to inflammatory diseases or prolonged inactivity is often associated with both oxidative and nitrosative stress. In this report, we critically review the experimental evidence that provides support for a causative link between oxidants and muscle atrophy. More specifically, this review will debate the sources of oxidant production in skeletal muscle undergoing atrophy as well as provide a detailed discussion on how reactive oxygen species and reactive nitrogen species modulate the signaling pathways that regulate both protein synthesis and protein breakdown.

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“…The calpain family of proteins is calcium dependent proteases that are important in the initiation of the breakdown of actin, myosin, and other structural proteins. Indeed, target pharmacological inhibition of calpain protects against disuse muscle atrophy (Tischler et al, 1990; Goll et al, 2003; Maes et al, 2007; Nelson et al, 2012; Talbert et al, 2013a). Caspase-3 is a member of the cysteine-aspartic acid protease family.…”

Section: Overview Of the Regulation Of Muscle Sizementioning

confidence: 99%

Can endurance exercise preconditioning prevention disuse muscle atrophy?

Wiggs

2015

Front. Physiol.

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Emerging evidence suggests that exercise training can provide a level of protection against disuse muscle atrophy. Endurance exercise training imposes oxidative, metabolic, and heat stress on skeletal muscle which activates a variety of cellular signaling pathways that ultimately leads to the increased expression of proteins that have been demonstrated to protect muscle from inactivity –induced atrophy. This review will highlight the effect of exercise-induced oxidative stress on endogenous enzymatic antioxidant capacity (i.e., superoxide dismutase, glutathione peroxidase, and catalase), the role of oxidative and metabolic stress on PGC1-α, and finally highlight the effect heat stress and HSP70 induction. Finally, this review will discuss the supporting scientific evidence that these proteins can attenuate muscle atrophy through exercise preconditioning.

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Calpain and caspase-3 play required roles in immobilization-induced limb muscle atrophy

Abstract: Talbert EE, Smuder AJ, Min K, Kwon OS, Powers SK. Calpain and caspase-3 play required roles in immobilization-induced limb muscle atrophy.

Cited by 81 publications

References 31 publications

From physical inactivity to immobilization: Dissecting the role of oxidative stress in skeletal muscle insulin resistance and atrophy

From physical inactivity to immobilization: Dissecting the role of oxidative stress in skeletal muscle insulin resistance and atrophy

Redox control of skeletal muscle atrophy

Can endurance exercise preconditioning prevention disuse muscle atrophy?

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