Sarcoplasmic reticulum: The dynamic calcium governor of muscle

Rossi, Ann E.; Dirksen, Robert T.

doi:10.1002/mus.20512

Cited by 186 publications

(156 citation statements)

References 200 publications

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“…As reviewed by Rossi and Dirksen (2006), developmental studies have shown that SAR exhibits a gradual increase during fibre maturation in both skeletal and smooth muscle. The biochemical Comparative immunoblot analysis of key Ca 2+ -handling proteins in young adult, adult and senescent rat skeletal muscle.…”

Section: Discussionmentioning

confidence: 99%

“…In addition, Ca 2+ -extrusion is mediated by the surface Na + /Ca 2+ -exchanger (NCX) and the plasmalemmal Ca 2+ -ATPase (PMCA). A physiological mediator between Ca 2+ -release and Ca 2+ -uptake is represented by the luminal SR Ca 2+ -reservoir system made up of calsequestrin (CSQ), sarcalumenin (SAR), junctate and related Ca 2+ -binding proteins (Rossi and Dirksen, 2006 (Leberer et al, 1990). Previous aging studies suggest that no major changes occur in SR protein expression levels in skeletal muscle, as reviewed by Margreth et al, 1999.…”

Section: Introductionmentioning

confidence: 99%

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Reduced expression of sarcalumenin and related Ca2+-regulatory proteins in aged rat skeletal muscle

O’Connell¹,

Gannon²,

Doran³

et al. 2008

Experimental Gerontology

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a b s t r a c tIn skeletal muscle, Ca 2+ -cycling through the sarcoplasm regulates the excitation-contraction-relaxation cycle. Since uncoupling between sarcolemmal excitation and fibre contraction may play a key role in the functional decline of aged muscle, this study has evaluated the expression levels of key Ca 2+ -handling proteins in senescent preparations using immunoblotting and confocal microscopy. Sarcalumenin, a major luminal Ca 2+ -binding protein that mediates ion shuttling in the longitudinal sarcoplasmic reticulum, was found to be greatly reduced in aged rat tibialis anterior, gastrocnemius and soleus muscle as compared to adult specimens. Minor sarcolemmal components of Ca 2+ -extrusion, such as the surface Ca 2+ -ATPase and the Na + -Ca 2+ -exchanger, were also diminished in senescent fibres. No major changes were observed for calsequestrin, sarcoplasmic reticulum Ca 2+ -ATPase and the ryanodine receptor Ca 2+ -release channel. In contrast, the age-dependent reduction in the a 1S -subunit of the dihydropryridine receptor was confirmed. Hence, this report has shown that downstream from the well-established defect in coupling between the t-tubular voltage sensor and the junctional Ca 2+ -release channel complex, additional age-related alterations exist in the expression of essential Ca 2+ -handling proteins. This may trigger abnormal luminal Ca 2+ -buffering and/or decreased plasmalemmal Ca 2+ -removal, which could exacerbate impaired signaling or disturbed intracellular ion balance in aged fibres, thereby causing contractile weakness.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Reduced expression of sarcalumenin and related Ca2+-regulatory proteins in aged rat skeletal muscle

O’Connell¹,

Gannon²,

Doran³

et al. 2008

Experimental Gerontology

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“…In the skeletal muscle, the sarcoplasmic reticulum (SR) functions as a dynamic Ca 2+ governor that provides automatic feedback control for altering and maintaining myoplasmic and SR Ca 2+ levels [50,51]. One of the proteins involved in Ca 2+ transport is the sarcoendoplasmic reticulum Ca 2+ -ATPase (SERCA) [52].…”

Section: Sercamentioning

confidence: 99%

Cachexia: a problem of energetic inefficiency

Argilés

Fontes-Oliveira

Toledo

et al. 2014

J cachexia sarcopenia muscle

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An alteration of energy balance is the immediate cause of the so-called cachexia. Although alterations of energy intake are often associated with cachexia, it has lately became clear that an increased energy expenditure is the main cause of wasting associated with different types of pathological conditions, such as cancer, infections or chronic heart failure among others. Different types of molecular mechanisms contribute to energy expenditure and, therefore, involuntary body weight loss; among them, adenosine triphosphate (ATP) consumption by sarcoplasmic reticulum Ca 2+ pumps could represent a key mechanism. In other cases, an increase in energy inefficiency will further contribute to energy imbalance.

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“…As a result of cross bridge cycling, actin filaments are pulled toward the center of the sarcomere, the sarcomere shortens, and the muscle contracts and generates force. The process is finally reversed upon cessation of calcium release following membrane repolarization and the subsequent reuptake of calcium into the SR through the activity of SR calcium ATPases (SERCAs) [3]. In addition to EC coupling, the triad also participates in the regulation of calcium homeostasis, which, in turn, regulates key cellular process such as oxidative stress, autophagy, and apoptosis.…”

Section: Introductionmentioning

confidence: 99%

Triadopathies: An Emerging Class of Skeletal Muscle Diseases

2014

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The triad is a skeletal muscle substructure responsible for the regulation of excitation-contraction coupling. It is formed by the close apposition of the T-tubule and the terminal sarcoplasmic reticulum. A rapidly growing list of skeletal myopathies, here referred to as triadopathies, are caused by gene mutations in components of the triad. These disorders, at their root, are caused by defects in excitation contraction coupling and intracellular calcium homeostasis. Secondary abnormalities in triad structure and/or function are also reported in several muscle diseases, most notably certain muscular dystrophies. This review highlights the current understanding of both primary and secondary triadopathies, and identifies important concepts yet to be fully addressed in the field. The emphasis of the review is both on the pathogenesis of triadopathies and their potential treatment.

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Sarcoplasmic reticulum: The dynamic calcium governor of muscle

Cited by 186 publications

References 200 publications

Reduced expression of sarcalumenin and related Ca2+-regulatory proteins in aged rat skeletal muscle

Reduced expression of sarcalumenin and related Ca2+-regulatory proteins in aged rat skeletal muscle

Cachexia: a problem of energetic inefficiency

Triadopathies: An Emerging Class of Skeletal Muscle Diseases

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