Reciprocal amplification of ROS and Ca(2+) signals in stressed mdx dystrophic skeletal muscle fibers. (Q42452644)

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26 January 2020

title

Reciprocal amplification of ROS and Ca(2+) signals in stressed mdx dystrophic skeletal muscle fibers (English)

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26 January 2020

3

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26 January 2020

Ernst Niggli

5

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26 January 2020

Natalia Shirokova

6

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26 January 2020

author name string

Vyacheslav M Shkryl

1

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26 January 2020

Adriano S Martins

2

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26 January 2020

Martha C Nowycky

4

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publication date

22 April 2009

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26 January 2020

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26 January 2020

volume

458

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issue

5

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26 January 2020

page(s)

915-928

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https://scigraph.springernature.com/pub.10.1007/s00424-009-0670-2

26 January 2020

exact match

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Uncontrolled calcium sparks act as a dystrophic signal for mammalian skeletal muscle

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Evidence of oxidative stress in mdx mouse muscle: studies of the pre-necrotic state

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RyR1 S-nitrosylation underlies environmental heat stroke and sudden death in Y522S RyR1 knockin mice

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Sarcolemmal damage in dystrophin deficiency is modulated by synergistic interactions between mechanical and oxidative/nitrosative stresses

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Regulation of capacitative calcium entries by alpha1-syntrophin: association of TRPC1 with dystrophin complex and the PDZ domain of alpha1-syntrophin.

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Effects of stretch-activated channel blockers on [Ca2+]i and muscle damage in the mdx mouse.

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Potential oxyradical damage and energy status in individual muscle fibres from degenerating muscle diseases

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Dynamic responses of the glutathione system to acute oxidative stress in dystrophic mouse (mdx) muscles

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Dystrophic cardiomyopathy: amplification of cellular damage by Ca2+ signalling and reactive oxygen species-generating pathways

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Utrophin-dystrophin-deficient mice as a model for Duchenne muscular dystrophy

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Hypernitrosylated ryanodine receptor calcium release channels are leaky in dystrophic muscle

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Effects of oxidation and reduction on contractile function in skeletal muscle fibres of the rat.

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Local calcium release in mammalian skeletal muscle.

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Extraocular, limb and diaphragm muscle group-specific antioxidant enzyme activity patterns in control and mdx mice

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Calcium, ATP, and ROS: a mitochondrial love-hate triangle

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Neuronal nitric oxide synthase and dystrophin-deficient muscular dystrophy

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Long-term study of Ca(2+) homeostasis and of survival in collagenase-isolated muscle fibres from normal and mdx mice

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A nitric oxide synthase transgene ameliorates muscular dystrophy in mdx mice

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A Ca(2+)-activated NADPH oxidase in testis, spleen, and lymph nodes

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N-Acetylcysteine ameliorates skeletal muscle pathophysiology in mdx mice

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Expression and modulation of an NADPH oxidase in mammalian astrocytes.

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Metabolic regulation of Ca2+ release in permeabilized mammalian skeletal muscle fibres.

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Impaired mitochondrial oxidative phosphorylation in skeletal muscle of the dystrophin-deficient mdx mouse.

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Invited Review: redox modulation of skeletal muscle contraction: what we know and what we don't

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Effects of S-glutathionylation and S-nitrosylation on calmodulin binding to triads and FKBP12 binding to type 1 calcium release channels.

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Genetic and pharmacologic inhibition of mitochondrial-dependent necrosis attenuates muscular dystrophy

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A transverse tubule NADPH oxidase activity stimulates calcium release from isolated triads via ryanodine receptor type 1 S -glutathionylation.

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Dystrophic heart failure blocked by membrane sealant poloxamer

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Myotube depolarization generates reactive oxygen species through NAD(P)H oxidase; ROS-elicited Ca2+ stimulates ERK, CREB, early genes

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Reactive oxygen species contribute to Ca2+ signals produced by osmotic stress in mouse skeletal muscle fibres.

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Increased activity of calcium leak channels caused by proteolysis near sarcolemmal ruptures

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Dystrophin and the membrane skeleton

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Dystrophin: the protein product of the Duchenne muscular dystrophy locus

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Mitochondrial redox state and Ca2+ sparks in permeabilized mammalian skeletal muscle

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Green tea extract decreases muscle necrosis in mdx mice and protects against reactive oxygen species

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A guide to sparkology: the taxonomy of elementary cellular Ca2+ signaling events.

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Oxidative stress as a potential pathogenic mechanism in an animal model of Duchenne muscular dystrophy

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TRPC3 and TRPC4 associate to form a redox-sensitive cation channel. Evidence for expression of native TRPC3-TRPC4 heteromeric channels in endothelial cells.

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Oxidative stress, chronic disease, and muscle wasting

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12 December 2020

Alteration in calcium handling at the subcellular level in mdx myotubes.

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12 December 2020

Mechanisms of stretch-induced muscle damage in normal and dystrophic muscle: role of ionic changes.

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12 December 2020

Evolution of the mdx mouse cardiomyopathy: physiological and morphological findings

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12 December 2020

Apoptosis precedes necrosis of dystrophin-deficient muscle

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12 December 2020

10.1007/S00424-009-0670-2

Identifiers

DOI

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26 January 2020

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