Cell Death and Oxidative Damage in Inflammatory Myopathies

Tews, Dominique S.; Goebel, Hans H.

doi:10.1006/clin.1998.4527

Cited by 70 publications

(57 citation statements)

References 47 publications

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“…Altered reduced/oxidized markers has been reported in MD patients and animal models (7,8,13,81). ROS produced in mdx mice and Col6a1 Ϫ/Ϫ mice might contribute to muscle pathology (80).…”

Section: Discussionmentioning

confidence: 99%

Mitochondrial Alterations and Oxidative Stress in an Acute Transient Mouse Model of Muscle Degeneration

Ramadasan-Nair¹,

Gayathri

Mishra³

et al. 2014

Journal of Biological Chemistry

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Background: Human muscular dystrophies and inflammatory myopathies share common pathological events. Results: The cardiotoxin (CTX) model displayed acute and transient muscle degeneration and all the cellular events usually implicated in human muscle pathology. Conclusion: Mitochondrial alterations and oxidative stress significantly contribute to muscle pathogenesis. Significance: The CTX model is valuable in understanding the mechanistic and therapeutic paradigms of muscle pathology.

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“…Altered reduced/oxidized markers has been reported in MD patients and animal models (7,8,13,81). ROS produced in mdx mice and Col6a1 Ϫ/Ϫ mice might contribute to muscle pathology (80).…”

Section: Discussionmentioning

confidence: 99%

Mitochondrial Alterations and Oxidative Stress in an Acute Transient Mouse Model of Muscle Degeneration

Ramadasan-Nair¹,

Gayathri

Mishra³

et al. 2014

Journal of Biological Chemistry

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“…Previous studies [17][18][19][20] have demonstrated iNOS overexpression in skeletal muscles of chronic heart failure patients and animals. Such iNOS overexpression has been shown to be induced by inflammatory cytokines and the priming effect of gamma interferone (γ-IFN) in chronic heart failure [21], iNOS overexpression has also been demonstrated in skeletal muscles of autoimmune inflammatory myopathies [22]. NOS activity inhibits mitochondrial respiration in skeletal muscles [23,24].…”

Section: Discussionmentioning

confidence: 99%

Endurance Exercise Training Attenuates the up Regulation of iNOS in the Skeletal Muscles of Chronic/Progressive Mouse Model of Parkinson’s Disease

Erekat

2013

J Neurol Res

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Background: Parkinson's disease (PD) is one of the most common neurodegenerative diseases in the elderly. PD complications include muscle weakness and fatigue, these complications lead in part to decrease the endurance of PD patients. Strength of skeletal muscles has a major role in ADL performance, which is one of the challenges that PD patients have. The main goals of this study are to study the expression of inducible nitric oxide synthase (iNOS) in the skeletal muscles of PD and to examine the effect of treadmill exercise training on iNOS expression in these skeletal muscles.

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“…NO also mediates denervation responses, inflammatory myopathy, aging, and neuromuscular transmission (Tews et al, 1997a,b;Capanni et al, 1998;Ribera et al, 1998;Tews and Goebel, 1998). Therefore, the collective effects of NO have a significant impact on muscle pathophysiology.…”

Section: Discussionmentioning

confidence: 99%

A Role for Nitric Oxide in Muscle Repair: Nitric Oxide–mediated Activation of Muscle Satellite Cells

Anderson

2000

MBoC

380

369

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Muscle satellite cells are quiescent precursors interposed between myofibers and a sheath of external lamina. Although their activation and recruitment to cycle enable muscle repair and adaptation, the activation signal is not known. Evidence is presented that nitric oxide (NO) mediates satellite cell activation, including morphological hypertrophy and decreased adhesion in the fiber-lamina complex. Activation in vivo occurred within 1 min after injury. Cell isolation and histology showed that pharmacological inhibition of nitric oxide synthase (NOS) activity prevented the immediate injury-induced myogenic cell release and delayed the hypertrophy of satellite cells in that muscle. Transient activation of satellite cells in contralateral muscles 10 min later suggested that a circulating factor may interact with NO-mediated signaling. Interestingly, satellite cell activation in muscles of mdx dystrophic mice and NOS-I knockout mice quantitatively resembled NOS-inhibited release of normal cells, in agreement with reports of displaced and reduced NOS expression in dystrophin-deficient mdx muscle and the complete loss of NOS-I expression in knockout mice. Brief NOS inhibition in normal and mdx mice during injury produced subtle alterations in subsequent repair, including apoptosis in myotube nuclei and myotube formation inside laminar sheaths. Longer NOS inhibition delayed and restricted the extent of repair and resulted in fiber branching. A model proposes the hypothesis that NO release mediates satellite cell activation, possibly via shear-induced rapid increases in NOS activity that produce "NO transients." INTRODUCTIONAfter muscle injury, satellite cells are activated and recruited to cycle as precursors for new muscle formation. Between injury and proliferation in vivo, satellite cells express immediate early genes after 3-6 h (Weiss, 1994;Kami et al., 1995) and muscle regulatory genes after 6 h (Grounds et al., 1992) in concert with proliferating cell nuclear antigen (Chambers and McDermott, 1996). The expression of these genes, release of growth factors such as bFGF, and DNA synthesis 24 -30 h later are used to characterize muscle regeneration in injured and dystrophic muscle (Grounds and McGeachie, 1989;Anderson et al., 1995;Floss et al., 1997 Floss et al., , 1998. The timing and sequence of events are specific to those of repair (Megeney et al., 1996;Li et al., 1997;McIntosh et al., 1998) but similar to those of development (Rudnicki and Jaenisch, 1995;Yun and Wold, 1996).The fine structure of satellite cells, positioned intimately between the fiber sarcolemma and the external lamina (Mauro, 1961;Ishikawa, 1966), changes during their transition from quiescence to activation. Nuclei enlarge and become euchromatic. The typical attenuated organelle-poor cytoplasm expands, and organelles such as mitochondria and rough endoplasmic reticulum hypertrophy (Schultz, 1976;Snow, 1977;Schultz et al., 1978Schultz et al., , 1985. However, although activation is recognized as essential to repair and defined as precursor s...

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Cell Death and Oxidative Damage in Inflammatory Myopathies

Cited by 70 publications

References 47 publications

Mitochondrial Alterations and Oxidative Stress in an Acute Transient Mouse Model of Muscle Degeneration

Mitochondrial Alterations and Oxidative Stress in an Acute Transient Mouse Model of Muscle Degeneration

Endurance Exercise Training Attenuates the up Regulation of iNOS in the Skeletal Muscles of Chronic/Progressive Mouse Model of Parkinson’s Disease

A Role for Nitric Oxide in Muscle Repair: Nitric Oxide–mediated Activation of Muscle Satellite Cells

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