Lipid Peroxidation Inhibition Blunts Nuclear Factor-κB Activation, Reduces Skeletal Muscle Degeneration, and Enhances Muscle Function in mdx Mice

Messina, Sonia; Altavilla, Domenica; Aguennouz, M.; Seminara, Paolo; Minutoli, Letteria; Monici, Maria C.; Bitto, Alessandra; Mazzeo, Anna; Marini, Herbert; Squadrito, Francesco; Vita, Giuseppe

doi:10.2353/ajpath.2006.050673

Cited by 107 publications

(100 citation statements)

References 46 publications

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“…The interplay between ROS and inflammation has also been supported by experiments in which mdx mice have been treated with anti-oxidant drugs, such as vitamin E analogue or N-acetylcysteine (NAC), demonstrating a reduced activation of NF-κB and an amelioration of dystrophic symptoms [105,106,109].…”

Section: Crosstalk Between Oxidative Stress and Inflammatory Responsementioning

confidence: 92%

“…In fact, NF-κB activation is induced by several inflammatory mediators, such as IL-1β, TNFα, and metalloproteinases, all molecules found elevated in DMD [57,[98][99][100][101][102]. Active NF-κB is able to translocate to the nucleus, inducing the expression of genes encoding for cytokines and chemokines, cell adhesion molecules, and matrix metalloproteinases [103][104][105][106][107].…”

Section: Crosstalk Between Oxidative Stress and Inflammatory Responsementioning

confidence: 99%

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Insights into the Pathogenic Secondary Symptoms Caused by the Primary Loss of Dystrophin

Forcina

Pelosi

Miano

et al. 2017

JFMK

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Duchenne muscular dystrophy (DMD) is an X-linked genetic disease in which the dystrophin gene is mutated, resulting in dysfunctional dystrophin protein. Without dystrophin, the dystrophin-glycoprotein complex (DGC) is unstable, leading to an increase in muscle damage. Moreover, the imbalance between muscle damage and repair leads to a chronic inflammatory response and an increase in the amount of fibrosis over time. The absence of dystrophin at the sarcolemma also delocalizes and downregulates nitric oxide synthase (nNOS) and alters enzymatic antioxidant responses, leading to an increase in oxidative stress. In this review, we analyze the pathogenic role of both inflammation and oxidative stress in muscular dystrophy.

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Section: Crosstalk Between Oxidative Stress and Inflammatory Responsementioning

confidence: 92%

Section: Crosstalk Between Oxidative Stress and Inflammatory Responsementioning

confidence: 99%

Insights into the Pathogenic Secondary Symptoms Caused by the Primary Loss of Dystrophin

Forcina

Pelosi

Miano

et al. 2017

JFMK

View full text Add to dashboard Cite

show abstract

“…Their study showed that PDTC treatment reduces the activation of NF-κB, muscle necrosis, and fatigue in mdx mice [58]. In addition, in vivo administration of IRFI-042, a potent antioxidant and inhibitor of lipid peroxidation, has been found to block the NF-κB activation and muscle degeneration and provide functional gain in mdx mice [59].…”

Section: Muscular Dystrophymentioning

confidence: 99%

Nuclear factor-kappa B signaling in skeletal muscle atrophy

2008

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Skeletal muscle atrophy/wasting is a serious complication of a wide range of diseases and conditions such as aging, disuse, AIDS, chronic obstructive pulmonary disease, space travel, muscular dystrophy, chronic heart failure, sepsis, and cancer. Emerging evidence suggests that nuclear factor-kappa B (NF-κB) is one of most important signaling pathways linked to the loss of skeletal muscle mass in various physiological and pathophysiological conditions. Activation of NF-κB in skeletal muscle leads to degradation of specific muscle proteins, induces inflammation and fibrosis, and blocks the regeneration of myofibers after injury/atrophy. Recent studies employing genetic mouse models have provided strong evidence that NF-κB can serve as an important molecular target for the prevention of skeletal muscle loss. In this article, we have outlined the current understanding regarding the role of NF-κB in skeletal muscle with particular reference to different models of muscle-wasting and the development of novel therapy.

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“…Increased forelimb strength normalized to weight and decreased fatigue reported. Reduced serum creatine kinase level also reported, indicating that oxidative stress/lipid peroxidation might be represented as one of the mechanisms activating NF-kappa B and the consequent pathogenetic cascade in mdx mice [18].…”

Section: Discussionmentioning

confidence: 99%

Dystrophin Degradation in Skeletal Muscles with Lipid Enrichment in Cattle

Jeon¹,

Kim

Lee³

et al. 2016

Journal of Life Science

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This study investigated the muscular dystrophin levels in freely moving Australian cattle mainly fed grass, freely moving Korean cattle fed mainly a grain diet, and Korean cattle fed a grain diet but housed in a relatively limited space of a cow house. The total skeletal muscle specimens of 244 cattle were collected and immediately fixed in 10% neutral formalin. The same area was biopsied from the cattle in both countries. The findings showed that fatty infiltration is highly correlated with membrane-associated protein degradation in skeletal muscle, and that among several membrane-associated proteins, dystrophin showed the most significant reduction in expression in the cattle with fatty infiltration. Similarly, CD36 was more highly expressed in the cattle with fatty infiltration of skeletal muscle. Various breeding factors, such as oxidative stress; the presence of oxidized lipids in the diet; and environmental factors such as exercise, temperature and amount of time spent, may have critical effects on the degradation of normal cytoskeleton proteins, which are required for maintaining normal skeletal muscle architecture. Among the sarcolemma membrane-associated proteins, dystrophin is the most sensitive membrane protein that is involved muscular dystrophy and muscular degeneration. Thus, the present findings may be useful for studies on muscular dystrophy in humans or the pathogenesis of muscular diseases in animal models.

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Lipid Peroxidation Inhibition Blunts Nuclear Factor-κB Activation, Reduces Skeletal Muscle Degeneration, and Enhances Muscle Function in mdx Mice

Cited by 107 publications

References 46 publications

Insights into the Pathogenic Secondary Symptoms Caused by the Primary Loss of Dystrophin

Insights into the Pathogenic Secondary Symptoms Caused by the Primary Loss of Dystrophin

Nuclear factor-kappa B signaling in skeletal muscle atrophy

Dystrophin Degradation in Skeletal Muscles with Lipid Enrichment in Cattle

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